Author Topic: ***CDC created this hybrid flu years ago--CDC/Baxter/Schering-Plough/Merck  (Read 91799 times)

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Offline TahoeBlue

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They've been tracking/working on this and known about this since 2004.... This is scary even for me.

"
The internal genes were of swine, human, and avian influenza virus origin, similar to those of contemporary U.S. cluster III H3N2 SIVs. The recovery of H3N1 is further evidence of reassortment among SIVs and justifies continuous surveillance.
"

http://www.encyclopedia.com/doc/1G1-127713245.html

Serologic evidence of human and swine influenza in Mayan persons.(Dispatches)
January 1, 2005
Antibodies against influenza viruses were detected in 115 serum samples from indigenous Mayan persons from Kochol, Yucatan. Seropositivity rates were 26.9% to A/Bayern/7/95, 40.8% to A/Sydney/5/97, 1.7% to A/Swine/ Wisconsin/238/97, and 79.1% to A/Swine/Minnesota/ 593/99.

This report is the first in Mexico of the prevalence of antibodies to swine influenza virus in humans.


http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1472084

Isolation and Genetic Characterization of New Reassortant H3N1 Swine Influenza Virus from Pigs in the Midwestern United States
Received July 26, 2005

Abstract

Since the introduction of H3N2 swine influenza viruses (SIVs) into U.S. swine in 1998, H1N2 and H1N1 reassortant viruses have emerged from reassortment between classical H1N1 and H3N2 viruses.

In 2004, a new reassortant H3N1 virus (A/Swine/Minnesota/00395/2004) was identified from coughing pigs. Phylogenetic analyses revealed a hemagglutinin segment similar to those of contemporary cluster III H3N2 SIVs and a neuraminidase sequence of contemporary H1N1 origin.

The internal genes were of swine, human, and avian influenza virus origin, similar to those of contemporary U.S. cluster III H3N2 SIVs.

The recovery of H3N1 is further evidence of reassortment among SIVs and justifies continuous surveillance.
....
In October 2004, a 1,000-head swine farm in Minnesota experienced a severe respiratory disease outbreak in 14-week-old pigs, which was characterized by coughing and increased mortality. The morbidity was approximately 80%, and the accumulated mortality reached 5% during the episode. Normal death loss in the index farm was less than 1% prior to the outbreak. Tissues from two dead pigs were submitted to the Veterinary Diagnostic Laboratory at the University of Minnesota for respiratory-disease diagnostic tests.
...

This suggests that A/Swine/Minnesota/00395/2004 H3N1 influenza virus is a reassortant containing genes from triple-reassortant H3N2 and contemporary H1N1 SIVs.
The clinical implications of this reassortant remain to be determined.

..

The recovery of an H3N1 subtype is further evidence of reassortment and antigenic shift in SIVs, justifying ongoing surveillance of animal populations for influenza A viruses that could represent a direct health threat, not only to swine populations, but also to humans. This study also demonstrated the usefulness of molecular technologies for such monitoring.


http://www.encyclopedia.com/doc/1G1-127713245.html

Serologic evidence of human and swine influenza in Mayan persons.(Dispatches)
January 1, 2005
Antibodies against influenza viruses were detected in 115 serum samples from indigenous Mayan persons from Kochol, Yucatan. Seropositivity rates were 26.9% to A/Bayern/7/95, 40.8% to A/Sydney/5/97, 1.7% to A/Swine/ Wisconsin/238/97, and 79.1% to A/Swine/Minnesota/ 593/99.

This report is the first in Mexico of the prevalence of antibodies to swine influenza virus in humans.
**********
Influenza virus type A has the capacity to infect humans, birds, swine, and other animals. Studies have repeatedly shown that influenza virus can move from 1 species to another

http://www.who.int/vaccine_research/diseases/influenza/Kistner.pdf

WHO Meeting on Development and Evaluation of Influenza Pandemic Vaccines, Geneva, November 2 – 3, 2005

Baxter‘s Serum Protein Free Vero Cell Technology

Titers of Different Influenza A Virus Strains of Human or
Animal Origin in Serum Protein Free Vero Cell Cultures:

Human A/PR/8/34 256
H1N1 Human A/USSR/90/77 256
Swine A/Swine/1976/31 256
Duck A/Duck/Bavaria/2/77 256
H2N2 Human A/Singapore/1/57 128
Human A/Hong Kong/1/68 128
H3N2 Swine A/Swine/Hong Kong/3/76 128
Swine A/Swine/Hong Kong/127/82 256
Duck A/Duck/Hong Kong/24/75 256
H5N3 Duck A/Duck/Singapore/3/97 256
H7N1 Fowl A/FPV/Rostock/34 256
H9N2 Fowl A/Quail/Hongkong/G1/97 128
Human A/Hongkong/1073/99 256
H5N1 Human A/Hong Kong/213/2003 256
A/Viet Nam/1203/2004 1024
A/Viet Nam/1194/2004 1024
A/SP83/2004 (Thailand) 512

Which says they can put these all together and hope for recombinations....

http://www.aasv.org/shap/issues/v8n2/v8n2p79.pdf  Diagnosis of swine influenza

keep finding more...  Swine vaccines for farms.... Humm...

http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1899867
2007 July;

Efficacy of swine influenza A virus vaccines against an H3N2 virus variant
Jee Hoon Lee, Marie René Gramer, and Han Soo Joo
Department of Veterinary Population Medicine, College of Veterinary Medicine, University of Minnesota

We compared the efficacy of 3 commercial vaccines against swine influenza A virus (SIV) and an experimental homologous vaccine in young pigs that were subsequently challenged with a variant H3N2 SIV, A/Swine/Colorado/00294/2004, selected from a repository of serologically and genetically characterized H3N2 SIV isolates obtained from recent cases of swine respiratory disease. The experimental vaccine was prepared from the challenge virus...

In the United States, H3N2 SIV isolates have been triple-reassortant viruses containing genes of human, swine, and avian lineages.
...
Reports from veterinary diagnostic laboratories also show an increasing number of H3N2 isolates with low serologic cross-reactivity to reference virus A/Swine/Texas/4199-2/98 antiserum. As well, there have been anecdotal reports from US swine operations of apparent vaccination failure with current commercially available bivalent SIV vaccines. Therefore, we investigated whether 3 commercially available bivalent vaccines provide satisfactory protection against an H3N2 variant of SIV.
...
Vaccination against SIV is now a routine method of respiratory disease control in swine farms because SIV has become 1 of the common causes of respiratory disease in pigs. The vaccines used are mostly bivalent, containing both H1N1 and H3N2 subtypes. Several cross-protection studies with various SIV vaccines in Europe and the United States have shown the vaccines to be effective under experimental conditions (15–20).

However, there have been debates on the efficacy of commercial SIV vaccines (7,15), since SIV isolates with antigenic and genetic diversity have been recovered from diseased pigs, and insufficient protection by the vaccines used on swine farms has been reported.

http://www.flutrackers.com/forum/showthread.php?t=12639

Vaccination of Pigs against Swine Influenza Viruses by Using an NS1-Truncated Modified Live-Virus Vaccine

Journal of Virology, November 2006, p. 11009-11018, Vol. 80, No. 22
0022-538X/06/$08.00+0 doi:10.1128/JVI.00787-06

Received 18 April 2006/ Accepted 22 August 2006

Swine influenza viruses (SIV) naturally infect pigs and can be transmitted to humans. In the pig, genetic reassortment to create novel influenza subtypes by mixing avian, human, and swine influenza viruses is possible.

An SIV vaccine inducing cross-protective immunity between different subtypes and strains circulating in pigs is highly desirable.

Here are the details on targets for commercial product sold by Schering Plough (although they don't give the exact composition of their vaccine)

http://www.xl3.info/
MAXIVAC EXCELL® 3
Like all of our swine products, MAXIVAC EXCELL® 3 is supported by a highly trained, experienced team of sales and technical service professionals who can assist with your vaccine decision-making.

http://www.intervet.com/

Intervet/Schering-Plough Animal Health is a global leader in the research, development, manufacturing and sale of veterinary medicines. We offer one of the industry's broadest, most innovative portfolios, spanning products for the prevention, treatment and control of disease in all major farm and companion animal species.

http://www.xl3.info/pdf/interview3.htm

http://www.ncbi.nlm.nih.gov/nuccore/9887193

  TITLE     Genetic characterization of H3N2 influenza viruses isolated from pigs in North America, 1977-1999: evidence for wholly human and
            reassortant virus genotypes

  JOURNAL   Virus Res. 68 (1), 71-85 (2000)

Just so people uunderstand the danger of "reassortment" and "Antigenic shift"

http://www.avian-influenza.com/Disease/intro/genetic_reassortment_through_antigenic_shift.asp

Genetic Re-assortment of Influenza A Viruses - 2008 Intervet/Schering-Plough Animal Health

Immunity against Influenza viruses

A host is infected with a particular influenza virus strain.
Antibodies are formed against that strain.
The antibodies formed protect the host against re-infection by the same virus strain.
The Emergence of “New Viruses” through Antigenic Shift and Drift

On the influenza virus, the surface proteins haemagglutinin and neuraminidase are important in inducing the formation of antibodies.

Changes in the surface proteins result in antigenic changes in the virus. The immune system no longer recognizes the virus strain and the host is susceptible to re-infection.

Influenza viruses can change in two different ways.

Antigenic drift
Gradual changes in an already circulating virus
Eventually the virus changes enough so that most of the population is susceptible to re-infection. There is then an influenza epidemic.
Size and severity of the epidemic is dependent on the degree to which the virus is different from those already experienced by the population.
Influenza viruses are constantly changing by antigenic drift
Type A and Type B influenza viruses undergo changes by antigenic drift.
The WHO Global Influenza Programme monitors antigenic changes and the adjustments required in influenza vaccines


Antigenic shift
The sudden emergence of new antigenically different influenza A sub-type.
The host population has no immunity against the new sub-type and an influenza pandemic follows.
Antigenic shift only occurs occasionally
Only Type A Influenza viruses change by antigenic shift
Antigenic shift is of public health concern as subtypes from different species may then be able to infect humans.
Mechanisms of Antigenic shift

Antigenic shift in man probably occurs through one of these mechanisms:

Direct transfer of a virus from another species.

Genetic re-assortment of avian and human influenza viruses infecting the same host. 

Believed to take place in pigs. See swine influenza.

New evidence indicates that it may also take place in humans.
The new virus that emerges may be an avian virus containing enough human influenza genes to allow human to human transmission.

Re-emergence of a virus that may have caused an epidemic years earlier.
For more information see:
The Center for Disease control and prevention, Influenza information. http://www.cdc.gov/flu/index.htm

....

So Schering-Plough  has animal health pharmaceutical  MFR in mexico... and R&D? Worldwide possibilities...

yes, they could handle the pandemic NWO contract job.
"Schering-Plough Pharmaceuticals is the worldwide pharmaceutical research and marketing unit of Schering-Plough Corporation "

http://www.prnewswire.com/cgi-bin/stories.pl?ACCT=104&STORY=/www/story/70050&EDATE=

President of Mexico Keynote Speaker As Schering-Plough Mexico Dedicates Pharmaceutical Manufacturing Facility

    XOCHIMILCO, Mexico, Feb. 28 /PRNewswire/ -- Mexican President Ernesto Zedillo was the keynote speaker at a ceremony held here today to formally dedicate Schering-Plough Corporation's (NYSE: SGP) new state-of-the-art manufacturing facility at the Xochimilco campus of the company's Schering-Plough Mexico subsidiary.

    The 100,000-square-foot, $50 million manufacturing plant provides Schering-Plough Mexico with the latest in facility and equipment design for producing a wide range of human and animal health pharmaceutical and health care products for sale in Mexico and Latin American countries.

    President Zedillo, addressing Schering-Plough employees, local officials, members of the medical community and guests at today's dedication ceremony, said, "I want to congratulate Schering-Plough and its employees on this new manufacturing facility.  The construction of this impressive facility during
difficult economic times for Mexico demonstrates Schering-Plough's commitment to scientific innovation and to providing unique products that meet the health care needs of today as well as those of the future."

    "The opening of this new manufacturing facility is an important milestone for Schering-Plough and our subsidiary in Mexico," said Alfredo M. Blanco, president, Latin America and Far East, Schering-Plough Pharmaceuticals.  "This plant represents a major capital investment for Schering-Plough and is a sign of the company's commitment to Mexico and our faith in the country's future economic development," he said.

    The new manufacturing facility meets Schering-Plough's Good Manufacturing Practice (GMP) requirements and U.S. and Mexico industry standards, and is designed to provide increased production capacity with the capability of handling a broad range of processes of varying complexity and scale.

    Several of the company's leading prescription products will be manufactured at the new facility, including the nonsedating antihistamine CLARITIN(R), the prostate cancer treatment EULEXIN(R) and many dermatological products.  The company will also manufacture several of its leading over-the-
counter products at the facility, including AFRIN(R) nasal spray, LOTRIMIN(R) antifungal products and COPPERTONE(R) sun care products.

    The Xochimilco facility, located on a 60-hectare site, features a three- story building that incorporates some of the most advanced facility design features available, including:
    -- High-quality architectural designs and surface finishes approaching "clean room" standards to minimize potential for product contamination;
    -- Solar orientation for maximum utilization of natural light;
    -- Vertical gravity feeding of bulk manufacturing materials for maximum energy efficiency;
    -- Utility systems that provide air, water and nitrogen of the highest purity for use in processing and operations;
    -- High-efficiency particulate air filtration and differential pressurization systems to produce and maintain a high-quality air supply for product manufacturing areas;
    -- Environmental safeguards, including high-efficiency natural gas boilers for reduced air emissions, dust collectors with terminal filtration for particulate material control, air exhaust systems and water treatment facilities new construction in Singapore, Shanghai and the United States.  These initiatives are increasing production capacity to meet future marketing needs in regions expected to experience the greatest growth, while also improving operating efficiency and reducing operating costs.
 
  Schering-Plough Pharmaceuticals is the worldwide pharmaceutical research and marketing unit of Schering-Plough Corporation of Madison, N.J., a research-based company engaged in the discovery, development, manufacturing and marketing of pharmaceutical and health care products worldwide.

http://www.thepoultrysite.com/poultrynews/14871/intervet-scheringplough-animal-health-appoints-executive-team
Intervet/Schering-Plough Animal Health appoints Executive Team
May 14, 2008
The new combination Intervet / Schering-Plough Animal Health strengthens the animal health portfolio in several areas and brings together complementary lines of pharmaceuticals, biologicals and innovative services. Intervet / Schering-Plough Animal Health is not only the world market leader in the production of animal health vaccines, but is also one of the world’s leaders in the field of animal health—with offices in more than 50 countries and products marketed in over 120 countries
Behold, happy is the man whom God correcteth: therefore despise not thou the chastening of the Almighty: For he maketh sore, and bindeth up: he woundeth, and his hands make whole ; He shall deliver thee in six troubles: yea, in seven there shall no evil touch thee. - Job 5

Offline TahoeBlue

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Oh and Merck is buying - merging with Schering-Plough

http://www.merck.com/newsroom/press_releases/corporate/2009_0309.html

03/09/2009
MERCK AND SCHERING-PLOUGH TO MERGE for 41.1 billion

– Infectious Disease:  Schering-Plough and Merck have complementary efforts in infectious disease.  The combined company will leverage the scientific and commercial strengths of both Schering-Plough and Merck in the treatment of Human Immunodeficiency Virus (HIV) and Hepatitis C Virus (HCV).  Schering-Plough's strong portfolio of HCV candidates, including boceprevir, is well-aligned with Merck's programs in this critical disease area.
 
– Women's Health:  Merck expects to benefit from a solid portfolio of women's health products including GARDASIL [human papillomavirus quadrivalent (types 6, 11, 16 and 18) vaccine, recombinant], a broad range of contraceptive options and biologic and small molecule fertility drugs, which will allow it to strengthen relationships with women's healthcare providers.

– Other Areas: Schering-Plough brings to the combined company a leading Animal Health business with strength in vaccines and small molecules, as well as many attractive consumer health brands such as CLARITIN, COPPERTONE, DR. SCHOLL'S and MIRALAX.
 
http://money.cnn.com/2009/03/09/news/companies/merck_schering_plough/?postversion=2009030909
 
Merck and Schering-Plough in $41B merger
Drugmaker to keep Merck name, and Merck CEO Clark will take reins



http://finance.aol.com/company/schering-plough-corporation/sgp/nys

Thomas J. Sabatino, Jr.  General Counsel
Mr. Sabatino joined Schering-Plough in 2004 as Executive Vice President and General Counsel. Mr. Sabatino was Senior Vice President and General Counsel of Baxter International, Inc. from 2001 to 2004
Behold, happy is the man whom God correcteth: therefore despise not thou the chastening of the Almighty: For he maketh sore, and bindeth up: he woundeth, and his hands make whole ; He shall deliver thee in six troubles: yea, in seven there shall no evil touch thee. - Job 5

Offline jesqueal

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Is this the correct conclusion:
Schering-Plough have the capacity to distribute contaminated Baxter vaccines in Mexico
And both groups have sufficient motivation and prior offences

Offline TahoeBlue

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Is this the correct conclusion:
Schering-Plough have the capacity to distribute contaminated Baxter vaccines in Mexico
And both groups have sufficient motivation and prior offences

Right....

1 Baxter develops re-assorted Swine-Avian-Human virus and gives a sample to Schering-Plough
2 Schering-Plough puts this virus into there farm Swine Flu vaccine distributed to Mexico
(they would need to cover there tracks a bit - random lots would contain the virus)
3 Pigs in Mexico spread the new virus to humans

No one would be able to tell the virus was manufactured.

http://en.wikipedia.org/wiki/Ernesto_Zedillo
Ernesto Zedillo Ponce de León (born December 27, 1951) is a Mexican economist and politician. He served as President of Mexico from December 1, 1994 to November 30, 2000

Zedillo currently works at Yale University in the United States, where he teaches economics and heads the Yale Center for the Study of Globalization
Behold, happy is the man whom God correcteth: therefore despise not thou the chastening of the Almighty: For he maketh sore, and bindeth up: he woundeth, and his hands make whole ; He shall deliver thee in six troubles: yea, in seven there shall no evil touch thee. - Job 5

Offline xundk

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I just read in a danish news article that Tamiflu vaccine is the only thing that can kill this bug, and I then did a bit of research/search... Scary shit, this vaccine...

http://www.naturalnews.com/023324.html

http://pulivahanan.wetpaint.com/page/A+Dangerous+Cure+for+a+Phony+Danger?t=anon

http://drbenkim.com/blog/2005/11/fda-taking-closer-look-at-anti.html

http://www.noonehastodietomorrow.com/eugenics/vaccines/901-901
Quote
In addition, as we have previously reported, those that have a stake in the Tamiflu vaccine include top globalists and BIlderberg members like George Shultz, Lodewijk J.R. de Vink and former Secretary of Defense Donald Rumsfeld.



Offline TahoeBlue

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I just read in a danish news article that Tamiflu vaccine is the only thing that can kill this bug, and I then did a bit of research/search... Scary shit, this vaccine...

http://www.naturalnews.com/023324.html
http://pulivahanan.wetpaint.com/page/A+Dangerous+Cure+for+a+Phony+Danger?t=anon
http://drbenkim.com/blog/2005/11/fda-taking-closer-look-at-anti.html
http://www.noonehastodietomorrow.com/eugenics/vaccines/901-901

Right again....

Oseltamivir is TamiFlu - Roche
Zanamivir is Relenza  - GlaxoSmithKline - Biota


http://forum.prisonplanet.com/index.php?topic=101338.msg603922#msg603922

http://www.cdc.gov/media/transcripts/2009/t090423.htm
(Navy Rear Admiral) Dr. Anne Schuchat:
...
The viruses are resistant to amantadine and rimantadine anti-viral drugs but they are sensitive or susceptible to oseltamivir and zanamivir, the newer anti-viral drugs for flu.


http://www.cdc.gov/flu/swine/recommendations.htm

Antiviral Treatment
Antiviral treatment for confirmed or suspected ill case of swine influenza virus infection may include either oseltamivir or zanamavir, with no preference given at this time. Recommendations for use of antivirals may change as data on antiviral susceptibilities become available.

I need to check the makers of oseltamivir and zanamavir

http://en.wikipedia.org/wiki/Oseltamivir

It was developed by US-based Gilead Sciences and is currently marketed by Hoffmann-La Roche (Roche) under the trade name Tamiflu. In Japan, it is marketed by Chugai Pharmaceutical Co., which is more than 50% owned by Roche. Oseltamivir is generally available by prescription only.

http://www.bhha.org.uk/zanamavir.htm

Zanamivir (Relenza) is a neuraminidase inhibitor that is licensed for the treatment of influenza in individuals over 12 years of age

http://www.relenza.com/

http://www.biota.com.au/

Biota is a leading anti-infective drug development company, based in Melbourne, Australia. Biota's initial success was the discovery of zanamivir, the first-in-class neuraminidase inhibitor

http://www.abnnewswire.net/press/en/60509/Biota_Holdings_Limited_(ASX:BTA)_Announced_Thier_Relenza_Royalty_for_March_2009_Quarter_At_A323_Million.html

Biota Holdings Limited (ASX:BTA) Announced Thier Relenza Royalty for March 2009 Quarter At A$32.3 Million

Melbourne, Apr 23, 2009 (ABN Newswire) - Biota Holdings Limited (ASX:BTA)(PINK:BTAHY) today announced that it had received notification from GlaxoSmithKline (LON:GSK) that Relenza sales were A$462 million and indicative royalties were A$32.3 million, for the three months ended 31 March 2009.

Indicative royalties for the nine months to 31 March 2009 total A$36.1 million.

Biota CEO Peter Cook attributed the performance to recent significant orders for pandemic stockpiling from the UK and Japanese Governments.

Link: http://www.abnnewswire.net/media/en/docs/60509-ASX-BTA-316895.pdf

About Biota Holdings Limited

Biota is a leading anti-infective drug development company based in Melbourne Australia, with key expertise in respiratory diseases, particularly influenza. Biota developed the first-in-class neuraminidase inhibitor, zanamivir, subsequently marketed by GlaxoSmithKline as Relenza.

Biota research breakthroughs have included a series of candidate drugs aimed at treatment of respiratory syncytial virus (RSV) disease, licensed to MedImmune Inc. and novel nucleoside analogues designed to treat hepatitis C virus (HCV) infections, licensed to Boehringer Ingelheim. Biota has clinical trials underway with its lead compound for human rhinovirus (HRV) infection in patients with compromised respiration or immune systems. In addition, Biota has a key partnership with Daiichi-Sankyo for the development of second generation influenza antivirals. Inverness Medical markets Biota's co-developed OIA FLU influenza diagnostics.

Relenza(tm) is a registered trademark of the GlaxoSmithKline group of companies.
BioStar(R) OIA(R) FLU and BioStar(R) OIA(R) FLU A/B are registered trademarks of Inverness Medical.
Behold, happy is the man whom God correcteth: therefore despise not thou the chastening of the Almighty: For he maketh sore, and bindeth up: he woundeth, and his hands make whole ; He shall deliver thee in six troubles: yea, in seven there shall no evil touch thee. - Job 5

Offline TahoeBlue

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If this turns out like the AIDS/HIV pandemic then the earliest cases of infection will be the most severe and deadly .... the virus will mutate into less deadly forms

http://www.digitaljournal.com/article/271523
CDC Briefs Media on Swine Influenza
...
At this time the CDC is looking for clusters of severe disease in the United States. This can be problematic as the flu mimics many other illnesses. Because of this it can take time to put the pieces of the puzzle together.

It is not known why the Mexican cases have been more severe than the reported US cases. They may be co-factors in this. It may also be that Mexico has yet to tag less severe cases and the United States has yet to tag more severe cases.


http://www.whale.to/v/keske3.html

EARLIEST AIDS, Part 4

FURTHER NOTE ON MUTATION RATE
 forgot last time to mention one other problem that I see in
the claims of early AIDS, in consideration of a steady and
rapid HIV mutation rate.

 ...
I would like to note that in general, an extremely high rate
of mutation tends to be regarded as a measure of instability,
and a sign of a YOUNG virus
.   I believe that the high
mutation rate should decrease in time
(I am looking for more
sources on this).  I may attempt some calculations, but it
seems to me that if HIV originated before 1959, given its high
mutation rate, we would have more than the 10 subtypes by now,
and they should have been detected earlier.
Behold, happy is the man whom God correcteth: therefore despise not thou the chastening of the Almighty: For he maketh sore, and bindeth up: he woundeth, and his hands make whole ; He shall deliver thee in six troubles: yea, in seven there shall no evil touch thee. - Job 5

Offline TahoeBlue

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Re: Swine Flu reassortment - Baxter - Schering-Plough - Merck connections
« Reply #7 on: April 25, 2009, 04:26:57 pm »
My speculation is that the original vector seems to be Minnesota  or Iowa

and Michael T. Osterholm, PhD, MPH Director, Center for Infectious Disease Research and Policy "is in place"

http://www.alumni.umn.edu/Living_with_Fear__Q_A_with_Michael_Osterholm.html

Living with Fear: Q&A with Michael Osterholm
By Shelly Fling

Michael Osterholm was just settling in as director of the new Center for Infectious Disease Research and Policy at the University of Minnesota when terrorists flew planes into the World Trade Center in New York, the Pentagon outside Washington, D.C., and a field in rural Pennsylvania. Overnight, as the nation’s vulnerability to terrorism became apparent, the former Minnesota state epidemiologist became one of the most sought-after experts in infectious diseases.

For years, Osterholm (M.S. ’78, M.A. ’80, Ph.D. ’80) has been an outspoken critic of the nation’s lack of preparedness in the face of bioterrorist threats. His book, Living Terrors: What America Needs to Know to Survive the Coming Bioterrorist Catastrophe (Delacorte Press, 2000), describes the havoc various types of biological warfare would wreak on an ill-prepared society. Osterholm has been called an alarmist, accused of exaggerating the likelihood of a large-scale bioterrorist attack on the United States. Nonetheless, he has been unwavering in his belief that people need to know the truth about the possibility of a widespread anthrax outbreak, smallpox epidemic, or other bioterrorist disaster. In short, he hopes to scare people into taking action.

And many are listening. Osterholm, 48, has been interviewed by every major media outlet in the United States since September 11. A former adviser on bioterrorism to the late King Hussein of Jordan, a U.S. ally, Osterholm recently testified before Congress about improving the public health system to respond to a bioterrorist attack and was named to a national advisory committee on bioterrorism by Tommy Thompson, the U.S. secretary of health and human services.

Although in his new advisory role he spends as much time in the nation’s capital as in Minnesota, Osterholm’s base will continue to be the University of Minnesota and the Center for Infectious Disease Research and Policy. "I think in some ways my entire career has been spring training for what’s happening right now," Osterholm says, "and the U has been a part of that for 26 years."

Q: Your book is a warning to the United States to prepare for an inevitable bioterrorist catastrophe. Suddenly, since the anthrax outbreaks following September 11, that time appears to be upon us. As a nation, how should we react given our lack of preparedness?
A: The current public health system, while it has been allowed to fray substantially over the past two decades, is still a system that is responding. How long they can respond and to what degree they can respond are important concerns, and we’re obviously going to need some real infusion of resources into that system.

People are confused by what we mean by "responding." They see the police, firefighters, and haz-mat workers responding to these anthrax letters, . . . but what they don’t see are the epidemiologists and the public health personnel who are doing the investigations and all of the lab testing that is so critical. That’s what we’re talking about in terms of responding. So when people ask if we’re unprepared, yes, we are unprepared. Are we totally unprepared? No, we’re really underprepared. And that’s what we need to respond to.

The events of September 11 have obviously been a watershed event. As tragic as it was in terms of loss of human life and this sense now of a newly found fear that we hadn’t had before, I think we as Americans also realize that we are going to have to change the way we look at terrorism, and we have changed the ways in which we have to prepare for it—for example, the discussions on the [federal government’s plan to stockpile] 300 million doses of smallpox vaccine. The public health capability at the federal, state, and local level is now receiving a renewed and fresh look in a way it hasn’t had in decades. And I think that’s very positive.

Q: Biological warfare has been a part of human history for centuries. In your book you cite an instance in 1346 in which the Tatar army attacked Caffa (in modern Ukraine) and catapulted the bodies of dead plague victims over the city wall. What is different about biological warfare today?
A: I have always been of the mind that, yes, you can take the complicated modern aerosol particle technology and transmit disease, but also the "box-cutter efficiency" for transmission is a reality. And think of the situation that occurred at Fort Pitt at the end of the French-Indian War, when the British troops actually gave smallpox blankets to the Delaware Indians and, over the next six months, largely decimated that population. Giving people blankets with the scabs of smallpox in the fibers—that’s not a high-tech weapon. It was a very powerful bullet and a very ineffective gun, but combined they still made a very effective weapon. Today, this anthrax, a material that’s currently available to someone, is a very very powerful bullet but has to date been used in a relatively ineffective gun. But if it gets into a semieffective gun, we’re in big trouble as a society.

We have to understand that that’s the reality today. That’s not fear mongering. You know, in early October I was on the various media outlets being interviewed, and look at how many people were on there saying again I was a fear mongerer, that people couldn’t possibly get their hands on this kind of anthrax, that it just didn’t exist, that it was just too technologically difficult, et cetera, et cetera. Now look where we’re at. And this is not about being right or wrong.

Q: You have a reputation of being a straight talker and have even been accused of perhaps needlessly scaring people, but do people have unfounded fears that you would like to quell?
A: We tend to approach this issue like a wide-swinging pendulum, where at one point, on September 10, bioterrorism just wasn’t an issue on the radar screen. Now the pendulum has swung all the way over to the side where we’re living in fear. Where the truth is . . . not quite in the middle, but a little on the fear side. We as a society have to adjust to this new world. A good example is that many different media outlets and elected officials blamed the Centers for Disease Control for the deaths of the two postal workers. I’ll tell you right now that, having been very outspoken on bioterrorism and having led some of the largest investigations in this country of infectious-disease outbreaks, had I been in the shoes of the CDC people on that given week, I don’t know if I’d have done anything differently either. Because the science just wasn’t there . . . the data weren’t there to suggest the danger.

We have to get off blaming people. . . . We have to understand what has happened to us and that we are now in a world where we’re going to have to adjust to military thinking of anticipated losses. . . . We are now going to have anticipated losses among our civilians, and we have to understand that. If we’re not prepared as a society to understand that, then when things get tougher we are not going to have the resolve to see it through. Failure is not an option here, so we’re going to have to figure out what to do.

And that’s not to scare people, but it’s to say you have a choice. You can either live in fear or live with fear. If we live in fear we will do nothing except be terrorized. If we live with fear, we’ll take all the American ingenuity that we have, we will understand the threat, we will bring the best of our biotechnology, we will bring the best of our public health and medical services systems, the best of our law enforcement, and we will go after it. That’s where academic health centers come in, and universities in general, because they’re going to be part of the solution. They’re going to be part of understanding how to live with fear. They will help us, with the American ingenuity, to respond.

If we do the other, if we allow ourselves to just sit there and blame people every time another person dies because of this, then we will live in fear and we will lose.

Q: In your book, you describe hypothetical bioterrorism events involving anthrax, food-borne disease, and smallpox and the results: thousands of deaths, mob scenes, and cities shutting down. How accurate is that estimation?
A: The food-borne one, that could happen tomorrow. The smallpox one, now we realize what the potential is for these programs. In some ways, where we’re at right now actually speaks very loudly that those scenarios are not far off at all. Look at what we’ve done, with just a couple of letters and a few cases of anthrax we’ve shut down all three branches of government. Think of if this were thousands of cases. Look at the panic and fear that’s been there. Was anything in that book exaggerated when you think about that? And that’s the problem. One of things I talk about is the fear and panic you have seen with just a few cases of illness. More people died of meningitis from natural causes over the same time period that these anthrax cases have occurred. But look at the fear and panic. Did you hear anything about the meningitis cases in the country? Not a thing.

Now imagine—and this is where the fear and panic will be escalated both in terms of what it will do to society but also as a result of many deaths—what if this is put into a much more effective gun and thousands of people die?

Q: What is your greatest concern regarding an outbreak of smallpox or other infectious disease?
A: The fact that panic and fear associated with infectious agents, and specifically bioterrorism agents, are so disproportionate with their actual risk to society of causing disease or death. And that’s one of the reasons they make very good bioweapons but also why we as a society have to prepare to respond. That’s the point I try to make in my book: One of the reasons you prepare and respond to this is not just due to the death and dying, it’s also because of what it does to society.

Q: People want to feel that they’re taking some kind of action, such as stockpiling food or buying gas masks. What do you think Americans should be doing as bioterrorism threats hang over them?
A: That’s one of the problems, that we don’t have anything per se for people to do, and that has left people feeling helpless. That’s why I have said contact your senators and congressmen and tell them what you believe about this issue, that this is really an important thing to you and you want them to respond, you want them to do something effective, you want them to provide leadership. That may seem shallow, but in fact it is truly an action you can take that could have tremendous implications.

You can ask your health plans and your hospitals and your health department, "How prepared are you?" You can go to your state legislators and ask, "What are the capabilities of our state?" What we’re not to do is give people platitudes. We’ve got to stop saying, "We’re OK; we’re fully prepared." I think anyone who in the past month has issued those words has regretted them.

Q: What, if anything, has been wrong with the U.S. response to the bioterrorism events?
A: Well, I think that we’ve got a ways to go. What I’m really pleased with, though, is that we are finally, for the first time, beginning to understand the need for comprehensive and long-term approaches to this, not just spin control and the message that we’re all OK. Messages that say that this is doomsday are not correct and also are not helpful.

Q: Do you have concerns that the U may have unwittingly helped train microbiologists who have since used their knowledge to develop bioweapons?
A: I don’t think we have any evidence of that. But I think it’s important that we understand that the balance between the freedom of the academic center and the potential for providing training to people who might one day use it for nefarious purposes is obviously a real issue, and it obviously needs real, very thoughtful discussion. I believe that the U is prepared to do that.

Q: What are you doing as an adviser to Health and Human Services Secretary Tommy Thompson?
A: All I can say is I appreciate the opportunity to help my country however I can right now, and because of my experience and my expertise I’ve been asked to provide input to the Bush administration. I’m actually on loan from the University, and that was a decision made by the U. . . . You know, the University has provided literally the most supportive environment for both this center and me specifically in terms of helping to respond to the bioterrorism issue. . . . From administrative support to public policy support, this university has been just incredible in how it’s assisted us in doing our job here. People probably don’t see the U as being right on the front lines here; but for the U we wouldn’t be on the front lines.

- Shelly Fling is editor of Minnesota.

http://online.krm.com/krm/10/docs/00279763/Osterholm.pdf

http://www.cidrap.umn.edu/cidrap/content/biosecurity/ag-biosec/news/dec2007swine.html
New swine flu virus supports 'mixing vessel' theory
Robert Roos  News Editor


Dec 20, 2007 (CIDRAP News) – A new influenza virus discovered in Missouri pigs has a combination of genes from avian and swine flu viruses, supporting the theory that pigs can serve as a mixing vessel for flu viruses and a potential source for a human pandemic strain, according to a report published yesterday.

Researchers found that the virus, an H2N3 subtype, caused illness in experimentally infected mice and was transmissible in swine and ferrets, suggesting it has adapted to mammals, according to the report, published in the Proceedings of the National Academy of Sciences (PNAS). In addition, genetic analysis showed the virus has a mutation linked with an increased ability to infect mammals.

The discovery marks the first identification of an H2 virus in swine, according to the authors of the report. The flu pandemic of 1957-58 was caused by an H2 virus, namely H2N2. That virus was replaced by an H3N2 strain in the pandemic of 1968-69, and H2 viruses have not circulated in humans since then. Hence, people younger than 40 have little immunity to H2 viruses, scientists say.

"Our results provide further evidence for the potential of swine to promote reassortment between different influenza viruses, and the genetic and biologic properties of the H2N3 viruses described suggest that it would be prudent to establish vigilant surveillance in pigs and in workers who have occupational exposure," states the PNAS report.

It was written by scientists from Iowa State University and the US Department of Agriculture's (USDA's) Agricultural Research Service (ARS), both in Ames, Iowa; the University of Minnesota in St. Paul; and St. Jude Children's Research Hospital and the University of Tennessee, both in Memphis. The lead author is Wenjun Ma of Iowa State and the USDA.

Two incidents 5 months apart
The discovery of the new virus began with an illness outbreak in pigs at a Missouri swine nursery in September 2006, according to the report. The pigs' lungs showed obvious signs of pneumonia, and tests showed the presence of an influenza gene, but the subtype could not be determined. Samples were submitted to the ARS in Ames, where genetic sequencing and a search of a flu sequence database showed the virus subtype to be H2N3.

After the virus was subtyped, a record search revealed that another unidentified virus had been submitted in April 2006, from a 12-week-old pig at another Missouri swine farm, according to the report. Analysis by the ARS showed that this isolate too was an H2N3, and the two viruses were nearly identical.

The two outbreak sites are about 8 miles apart, according to Marie Gramer of the University of Minnesota College of Veterinary Medicine in St. Paul, a coauthor of the report. She said there was no connection between the two operations.

Phylogenetic analysis showed that the virus's hemagglutinin (HA) gene most closely matched the genes of H2 viruses isolated from North American mallard ducks, while the neuraminidase (NA) gene was closely related to that of an H4N3 virus found in blue-winged teal. Five of the other six genes were derived from swine flu viruses currently circulating in the United States, the scientists determined.

The source of the virus is unknown, but the likeliest possibility is pond water, which was used to clean barns and water the animals on both farms, according to the report. That transmission pathway has been described before.

Looking for genetic evidence of the new viruses' adaptation to mammals, the authors compared their HA genes with the HA genes from avian H2N3 viruses. They found an amino-acid substitution at position 226 that, in other H2 and H3 viruses, has been associated with adaptation of avian viruses to humans, according to the report.

To assess the new isolate's pathogenicity in swine, the scientists inoculated 20 4-week-old pigs with one of the viruses, and 3 days later housed 10 other pigs with the inoculated pigs. On necropsy, the inoculated pigs were found to have mild to moderate pneumonia, while the contact pigs had antibodies to the virus but slight or no signs of pneumonia.

The researchers also exposed mice to one of the H2N3 viruses at three different doses. Mice that received the middle or highest doses showed signs of illness, and 75% of those with the highest dose died, but none exposed to the lower doses died.

To test the virus's effect in ferrets, the scientists inoculated three 18-week-old, separately caged ferrets with it and then placed an uninfected ferret in each cage a day later. Subsequent tests showed the virus was present in all the animals, but none showed obvious signs of illness.

Reason for public health concern
The authors write that their findings are "of considerable concern to public health." In particular, the H2N3 viruses' mutation associated with an affinity for human-type cell-surface receptors and their ability to replicate and spread in swine and ferrets "suggests that the swine H2N3 viruses have undergone adaptation to the mammalian host and as such have the ability for sustained transmission."

However, the report also says that "receptor-binding changes" are not sufficient by themselves to permit avian flu viruses to successfully adapt to humans. For example, swine H1N1 flu viruses prefer human-type receptors and have occasionally infected humans but have not become established in human populations.

Gramer told CIDRAP News that no illnesses were reported among farm workers in connection with the swine cases, and no workers were tested at the time. However, serologic testing of the workers is currently being conducted under a grant from the Centers for Disease Control and Prevention, she reported.

When asked whether the newfound virus currently represents a threat to humans, Gramer replied, "No more than any other influenza virus in the world. Transmission of flu from pigs to humans is likely rare. This flu itself is rare and we don't know if it is currently circulating in this farm or any other farm in the USA. We haven't found it again."

Although pigs have long been regarded as a viral mixing vessel that could potentially produce human pandemic strains, whether this has ever happened is unclear, the PNAS report states. The 1957 and 1968 pandemic viruses both resulted from genetic reassortment of human and avian strains, but the mixing might have occurred in humans, pigs, quail, or some other host, it says.

Gregory C. Gray, MD, MPH, an Iowa infectious disease expert who was not involved in the study, says the new findings should cause public health officials "much concern" and point up the need for careful and coordinated flu surveillance in swine, poulty, and humans who work with them.

The report suggests that state and federal public health officials should work "aggressively" with the swine and poultry industries to study the prevalence of the new virus and find out whether it is infecting humans and to set up coordinated surveillance programs, said Gray, who is director of the Center for Emerging Infectious Diseases at the University of Iowa in Iowa City.

Much effort is currently devoted to the hunt for highly pathogenic flu viruses in migratory and aquatic birds, Gray continued. "Influenza surveillance in agriculture is largely managed by the industries. Our agriculture industry and human influenza surveillance are not well coordinated. We might wake up one day to find a virus like the one in this report has become endemic in our agriculture industries and a major threat to the industries as well as to man."

He added that numerous reports show that common swine flu viruses can cause severe disease in humans. "A novel virus like the one in the PNAS report, if highly transmissible between people, has potential to cause markedly more morbidity, even a pandemic," he said.

Gray has previously written about the need to include agricultural workers in seasonal flu vaccination programs, flu surveillance, and pandemic planning. "The PNAS report greatly increases our concern," he commented.

Another expert, Michael T. Osterholm, PhD, MPH, generally concurred with Gray. "I think it’s a potentially serious threat," said Osterholm, director of the University of Minnesota Center for Infectious Disease Research and Policy, publisher of CIDRAP News. "I think one of the problems we have is that we tend to think of influenza today, because of H5N1, as an Asian disease, with the roots of any future pandemic planted deep in Asia. But we have to be very careful because we don't know that."

Gramer commented that flu is very common in pigs, particularly in the spring, fall, and early winter, and is typically mild and self-limiting. "Flu surveillance in pigs is entirely voluntary," she said. Some surveillance for flu in farm workers is carried on under research grants from the CDC and the National Institutes of Health, she added.

Ma W, Vincent AL, Gramer MR, et al. Identification of H2N3 influenza A viruses from swine in the United States. Proc Natl Acad Sci 2007 Dec 26;104(52):20949-54 [Abstract
Behold, happy is the man whom God correcteth: therefore despise not thou the chastening of the Almighty: For he maketh sore, and bindeth up: he woundeth, and his hands make whole ; He shall deliver thee in six troubles: yea, in seven there shall no evil touch thee. - Job 5

Offline TahoeBlue

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Since the introduction of H3N2 swine influenza viruses (SIVs) into U.S. swine in 1998, H1N2 and H1N1 reassortant viruses have emerged from reassortment between classical H1N1 and H3N2 viruses.

Ok Introduction? what?

"In August of 1998, a North Carolina herd exhibiting clinical signs of influenza was identified with H3N2 SIV"

NO explanation where IT CAME FROM!!!!!

http://www.unipr.it/arpa/facvet/dip/dipsa/ric/prrs2003/265-266.pdf
4th International Symposium on Emerging and Re-emerging Pig Diseases – Rome June 29th – July 2nd, 2003
ATTENUATION OF AN H3N2 SWINE INFLUENZA VIRUS UTILIZING A REVERSE GENETICS APPROACH

Swine influenza (SI) is an acute respiratory disease of swine caused by type A influenza viruses. Before 1998, mainly “classical” H1N1 SI viruses (SIV) were isolated from swine in the United States (1,2). Since then, antigenically distinct reassortant H1- and H3-SIVs have been identified as causative agents of respiratory disease in pigs on U.S. farms (3,4,5). The H3N2 SIVs currently circulating in U.S. swine populations are triple reassortant viruses containing avian-like (PA, PB2), swine-like (M, NP, NS) and human-like (HA, NA, PB1) gene segments (4,5). Genetic characterization of swine influenza viruses isolated in the last 2 years has shown that these H3N2 viruses have undergone further reassortment with the classical H1N1 viruses resulting in novel H1N2 and H1N1 SIVs.

http://www.pork.org/PorkScience/Documents/swineinfluenza.pdf

Swine Influenza Virus
Background: Swine influenza virus (SIV) infections in swine are common causes of respiratory
disease in pigs. Infection of pigs occurs throughout the world. Prior to 1998, swine influenza in pigs
in the United States was caused by H1N1 SIV. In August of 1998, a North Carolina herd exhibiting
clinical signs of influenza was identified with H3N2 SIV. Since that time, isolates from pigs in Texas,
Iowa, Minnesota, and Illinois have been typed as H3N2 SIV.



Etiology: Swine influenza virus is an orthomyxovirus with a segmented RNA genome.
Orthomyxoviruses are divided into three groups as type A, type B, or type C. Only type A viruses
infect pigs. The type A viruses are further subtyped based on their hemagglutinin (H) and neuraminidase
(N). There are 15 hemagglutinins (H1-H15) and 9 neuramindases (N1-N9) that have been
identified in humans, animals, and birds.
Due to the segmented genome, genetic reassortment can
occur between different subtypes, resulting in antigenic shift when H and N genetic material are
exchanged between viruses. In addition, antigenic drift can occur due to accumulation of point
mutations in genetic material, which is common in RNA viruses.


Pathogenesis: Viral replication is generally restricted to the respiratory tract of the pig. The primary
area of infection is the respiratory epithelium lining the airways. Immunity to infection develops
very rapidly and is detectable by the hemagglutination-inhibition test around 6-7 days post-infection,
which provides a very narrow window of time for diagnosis by nasal swab specimens. Only pigs with
acute disease should be swabbed for virus detection. Typically, those pigs are febrile with high temperatures
of 105oF or higher, and are off feed (sows or boars) or are reluctant to move at all (nursery
pigs).

Epidemiology: Two forms of disease occur in swine, endemic or epidemic (epizootic). Sow herds
with endemic H1N1 or H3N2 influenza will ordinarily have sporadic abortions (due to the high fever
associated with acute infection) and may also be manifested as a decreased conception rate due to
first and second trimester abortions that are recorded as “not in pig” events. Aborting sows will usually
be off feed for 2 to 3 days with a fever of 105oF. Epidemic influenza is readily apparent in all age
groups. Onset of disease is acute and dramatic, particularly in the sow herd. For naive sow herds,
abortion may be widespread, ranging from 5 to 10% of the sow herd. Unlike PRRS-induced abortion,
influenza-induced abortion storms resolve within 2 to 3 weeks. Spread is rapid, typically sweeping
a breeding/gestation facility within a week. Similarly, the respiratory disease associated with epidemic
influenza in growing pigs is of rapid onset, and the initial viral pneumonia-induced coughing
within the herd is of short duration due to rapid spread among susceptible pigs. Transmission is by
direct contact and highly infectious viral aerosols within facilities. Under appropriate environmental
conditions, airborne spread may result in explosive spread among farms within very dense swine production
areas. Unless appropriate management decisions and interventions are made, herds with
acute or epidemic disease very commonly have endemic disease thereafter.
Epidemic disease is seasonal in nature, and peaks in periods of greatest environmental stress, such
as the late fall and winter months of the Midwest, or late summer in the Southeast. Disease onset
often occurs during extreme temperature fluctuations. Commonly, it is associated with chilling that
can occur in the Midwest due to dramatic drops in outdoor temperature or loss of heating, and in the
Southeast due to malfunctioning drip cooling systems that remain on into the evening in combination
with the increased ventilation rates of summer.

The incidence of H3N2 influenza in the US swine herd is unknown at this time. The relatively simultaneous detection of infected herds in the Southeast and Midwest in late 1998 infers that H3N2 was introduced into the US swine herd at least 6 months prior to the initial detection reported from North Carolina. Isolation of H3N2 influenza virus from herds vaccinated against H1N1 influenza has been a common occurrence in the Midwest (Illinois, Iowa and Minnesota) and the Southeast (North Carolina). It is likely that the prevalence of H3N2 and H1N1 in infected US swine herds is now similar to Europe, with a slightly higher prevalence of H1N1 than H3N2, 60% vs. 40%. A national, industry wide serologic survey will be needed to determine
the actual prevalence.

Risk of transmission of this new type of influenza virus (in the US) to people is probably minimal for the strains of H3N2 virus circulating in US swine at this time. The initial isolate from North Carolina was neutralized with hyperimmune sheep antiserum against a Chinese 1995 human H3N2 isolate. It is very likely that most people already have immunity against later (1996, 1997 or 1998) human strains of H3N2, which in turn provides solid protection against the H3N2 influenza currently circulating in US swine.

Clinical Signs: Pigs infected with H1N1 SIV usually can not be differentiated from pigs infected with H3N2 SIV based on clinical signs as they are similar with both infections. Field reports suggest that H3N2 SIV infections are more severe than H1N1 SIV infections. This is probably due to the fact that many pigs are vaccinated with H1N1 SIV vaccines or already have antibodies due to natural infection with H1N1 SIV and, therefore, should be protected from severe clinical signs due to H1N1 SIV infection. Pigs infected with SIV show a variety of clinical signs including coughing, nasal and/or ocular discharge, sneezing, depression, anorexia, dyspnea, and hyperthermia. It is not uncommon for pigs to develop temperatures of >105o F.

Reproductive performance in both males and females can be affected by SIV infections. Elevated rectal temperatures in boars can result in adverse effects on the testicles and sperm, resulting in reduced fertility. Depending on the stage of gestation, affected females can show a variety of reproductive problems including delayed return to estrus, abortions, and reduced viability of piglets at birth. Milk production in lactating females may be reduced, resulting in adverse effects on the nursing piglets.

Diagnosis: Swine influenza virus infections can be diagnosed based on a combination of clinical signs, typical gross and histopathologic lesions, diagnostic tests to detect live virus, nucleic acid, or antigen and serologic assays. Type A influenza viruses share a common matrix protein and nucleoprotein. Consequently, there can be some cross reactivity with H1N1 and H3N2 SIV in some tests, such as ELISA or indirect  immunofluorescence assay (IFA), due to the common proteins. Tissues, particularly lung, can be evaluated for the presence of live or inactivated virus using immunohistochemistry, fluorescent antibody techniques, and commercially available antigen capture ELISAs which detect type A influenza viruses. The presence of
SIV or viral antigen can also be evaluated from nasal or lung airway swabs on the antigen capture ELISAs. The presence of SIV nucleic acid in diagnostic specimens can be evaluated by polymerase chain reaction (PCR). Virus can be isolated from tissues or swabs in cell cultures or embryonating chicken eggs. Virus isolates can be typed to determine the H and N components, which is important for determining the type(s) of SIV vaccine to use in a herd.

Swine influenza virus has the ability to cause red blood cells to agglutinate. When type-specific antibodies are present, hemagglutination is inhibited. This phenomenon is taken advantage of through the use of a hemagglutination-inhibition (HI) serology test for detection of SIV antibodies. Since this phenomenon is based on the H component of the virus, a single HI test can not be used to detect both H1 and H3 antibodies as different viruses have to be used in the test. Additional assays for detecting H1N1 or H3N2 SIV antibodies include the ELISA, immunodiffusion, and IFA.

Treatment/Prevention/Control: Treatment for SIV infections is based on supportive therapy and can include reducing stress, medication to lower body temperatures, and ensuring the pig is made as comfortable as possible. Prevention is based on good management practices to reduce the risk of SIV entering the herd and include good biosecurity measures such as limiting people and vehicle traffic on the premise, properly cleaning and disinfecting trucks that take pigs to market, and quarantining new pigs before placing them in the general pig population of the farm. Due to the antigenic differences between H1N1 SIV and H3N2 SIV, vaccines containing H1N1 SIV are not expected to be protective with H3N2 SIV infections.

Therefore, an H3N2 vaccine will need to be used. Options for vaccination include autogenous or commercially available vaccines.

References:
Easterday BC and Van Reeth K. 1999. Swine Influenza. Pages 277-290 in Diseases of Swine. Iowa State University Press. Ames, Iowa.
Fenner F, Bachmann PA, Gibbs EPJ, Murphy FA, Studdert MJ, and White DO, eds. 1987. Orthomyxoviridae. Pages 473-484 in Veterinary Virology.
Academic Press, Inc. San Diego, California.
1National Veterinary Services Laboratories, Ames, IA
2Rollins Animal Disease Diagnostic Laboratory, Raleigh, NC

http://www.ipic.iastate.edu/reports/00swinereports/asl-689.pdf
Iowa State University Health
Characterization of H3N2 Swine Influenza Viruses in Iowa Swine

Summary and Implications
Since December 1998 when swine influenza virus (SIV) with H3N2 was first identified in Iowa swine, prospective and retrospective studies were conducted to monitor and evaluate H3N2 SIV infections in swine population in Iowa until February 2000. A serological survey revealed that H3 SIV had been widely spread in Iowa swine within first 6 months after initial identification and that both H1 and H3 SIV coexited. Many herds tested had the evidence that animals were exposed to both subtypes of SIV. In some cases, both subtypes were isolated from the same animal. All circumstantial evidences strongly suggested the emergence of new subtype due to reassortment of H1N1 and H3N2 strains;
however, no evidence of new reassortant was yet found in Iowa during this study period. A one-way hemagglutination inhibition (HI) assay on banked field isolates of H3N2 SIV demonstrated that the majority of field isolates were antigenically conserve. These observations suggest that diagnostic assays using an initial Midwest H3N2 SIV isolate should be reliable for
diagnosing infection of H3N2 SIV. This observation also suggests that a vaccine using an initial Midwest H3N2
SIV may provide reliable cross protection against a variety of H3N2 strains. However, a few isolates were
found resistant to HI activity conferred by antiserum raised against a H3N2 Midwest isolate, warranting a continuous
surveillance for antigenic drift among isolates.

Introduction
Influenza is a common respiratory disease of swine in most of the swine-producing regions throughout the
world. Since 1918, when the first cases of swine influenza were discovered in the United States (3), the predominant
subtype that has affected pigs in the United States has been the classic H1N1 (2). This strain is similar
genetically and antigenically to the type A virus implicated in “Spanish Flu” (4).

However, since December 1998 and January 1999, a H3N2 subtype of swine influenza virus (SIV) was isolated from clinically affected swine in Iowa (IA), Minnesota, North Carolina (NC), and Texas (TX). A genetic analysis demonstrated that Midwest isolates (IA, MN, TX) and NC isolate were distinct (5).

Herein, prospective and retrospective observational studies were conducted on Iowa swine to 1) assess the prevalence of H3N2 SIV infections; 2) determine/monitor the emergence of NC genotype and new reassortant; and 3) characterize the antigenic stability of H3N2 SIV isolates.

Results and Discussion

Influenza outbreaks by H3N2 SIV were initially identified in swine operations at northwestern part of Iowa and quickly
spread to herds in other parts of the state
. In June, the serological survey on finishing pigs revealed that 64% of pigs
and 92% of herds were serologically positive for the Midwest H3N2 virus, indicating that H3N2 SIV was already
widespread throughout the Iowa swine population. About 30% of swine tested had antibodies for both H1 and H3 SIV,
showing that both strains were circulating in swine herds at the same time. It suggested the risk for the emergence of new
subtype(s) due to reassortment between H1N1 and H3N2.


However, neither new reassortant nor NC genotype was identified during this study. Antigenically, hemagglutinin
(HA) of the majority (96.7%) of H3N2 SIV isolates tested appeared to be stable; however, a few isolates (N=4) were
significantly resistant to HI activity by both TX and NC antisera.

Collectively, these results demonstrate that H3N2 strains of SIV are of significance to the veterinary profession. Our
observations also indicate that both H1 and H3 subtypes will co-exist as significant pathogen
.

High seroprevalence of H3N2 in Iowa justifies the need for an effective vaccine to control swine influenza, as was the case for H1N1 SIV. The relatively good antigenic stability of HA protein among field isolates suggests that vaccines and diagnostic tests using an initial Midwest H3N2 SIV isolate should provide reliable crossprotection against H3N2 strains and be reliable for diagnosing the respiratory disease by H3N2 SIV, respectively.

Nevertheless, a continuous surveillance for the emergence of new subtype(s) should remain effective. Identification of a few HI resistant isolates warrants further investigation on the antigenic drift among isolates as it was the case in Europe (1)
Behold, happy is the man whom God correcteth: therefore despise not thou the chastening of the Almighty: For he maketh sore, and bindeth up: he woundeth, and his hands make whole ; He shall deliver thee in six troubles: yea, in seven there shall no evil touch thee. - Job 5

Offline TahoeBlue

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Baxter is ready to produce The Global pandemic vaccine supplies...

HN51 'accidentally' mixed in Flu Vac.. WTF?

About CELVAPAN

CELVAPAN is manufactured in a cell culture-based system in Bohumil, Czech Republic, at one of the largest cell culture vaccine production facilities in the world. Vero cell technology uses a well-established cell line originally derived from African green monkey kidneys in 1962. A continuous cell line has been derived from these cells so that an unlimited supply of cells is available without the requirement of generating additional cells from animals.

The same monkey cells used in the polio vaccines with SV40


http://www.redorbit.com/news/health/560745/baxter_initiates_clinical_study_with_cellbased_candidate_h5n1_pandemic_vaccine/index.html

Baxter Initiates Clinical Study With Cell-Based Candidate H5N1 Pandemic Vaccine
Posted on: Wednesday, 5 July 2006, 18:00 CDT
...

Baxter is developing both seasonal (or inter-pandemic) and pandemic influenza vaccines based on the company's proprietary vero-cell technology, which has the potential to significantly reduce production time compared to traditional vaccine production methods that use embryonated hens' eggs. The company is already licensed to produce vaccines at its commercial scale cell- culture vaccine manufacturing facility in Bohumil, Czech Republic, which is GMP approved and fully validated to Biosafety Level Three (BSL-3).

Cell-based systems for production of vaccines offer a number of potential benefits over more traditional egg-based systems. Baxter's vero-cell technology is capable of producing high yields of influenza virus without the addition of any animal-derived serum. Through the company's research and development work, Baxter has been successful in growing wild-type virus at pilot and commercial scales using its unique vero-cell technology. This means the company is currently capable of manufacturing pandemic vaccine without having to wait for high-growth or attenuated virus reassortants normally used when vaccine is produced in eggs. The requirements for such reassortants may involve considerable delay in vaccine production in the event of a pandemic.

In addition, Baxter is working with the U.S. National Institute of Allergy and Infectious Diseases (NIAID), in partnership with Fisher BioServices Inc., and with the U.S. Department of Health and Human Services in partnership with DVC LLC, a Computer Sciences Corporation Company, to develop vero-cell based H5N1 pandemic and seasonal influenza candidate vaccines.

Both collaborations are the result of U.S. Government contract awards. Baxter and its partners will be providing the vero-cell based candidate vaccines to the agencies for further clinical testing in the United States, which is expected to begin later in 2006 and 2007.

Baxter is currently in discussions with several other governments regarding its candidate pandemic vaccine, and has been awarded a contract to supply two million doses of cell-culture based candidate H5N1 vaccine to the U.K. government.

Behold, happy is the man whom God correcteth: therefore despise not thou the chastening of the Almighty: For he maketh sore, and bindeth up: he woundeth, and his hands make whole ; He shall deliver thee in six troubles: yea, in seven there shall no evil touch thee. - Job 5

Offline TahoeBlue

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Nice sum-up of the History of H3N2. No one even trys to explain where it came from in 1998....

It also shows that something significant occured in 2005 with H3N2

http://www.cdc.gov/ncidod/EiD/vol12no07/06-0268.htm
Emerging Infectious Diseases
Triple Reassortant H3N2 Influenza A Viruses, Canada, 2005

Since January 2005, H3N2 influenza viruses have been isolated from pigs and turkeys throughout Canada and from a swine farmer and pigs on the same farm in Ontario. These are human/classical swine/avian reassortants similar to viruses that emerged in US pigs in 1998 but with a distinct human-lineage neuraminidase gene


Influenza viruses of the classical H1N1 lineage were the dominant cause of influenza among North American pigs for >60 years (1). However, in 1998, H3N2 viruses emerged and rapidly spread throughout the US swine population (2–4). These were unique triple reassortant genotype viruses, with hemagglutinin (HA), neuraminidase (NA), and RNA polymerase (PB1) genes of human influenza virus lineage; nucleoprotein (NP), matrix (M), and nonstructural (NS) genes of classical swine virus lineage; and RNA polymerase (PA and PB2) genes of North American avian virus lineage.

Further reassortment between these viruses and classical H1N1 swine viruses led to the emergence of reassortant H1N2 and H1N1 viruses among pigs in the United States (1).

The reassortant H3N2 and H1N2 viruses have also been isolated from turkeys and ducks in the United States (5–8). Despite geographic proximity and cross-boundary trade in pigs and turkeys between the United States and Canada (9, D. Harvey, pers. comm.), these reassortant viruses did not initially infect animals in Canada.

However, beginning in approximately January 2005, H3N2 influenza viruses swept rapidly across Canada. We describe the genetic characterization of reassortant H3N2 viruses from pigs, turkeys, and a swine farm worker in contact with sick pigs during this outbreak.
....
Conclusions
To our knowledge, this report describes the first isolation of a human/classical swine/avian triple reassortant H3N2 virus from a human. This isolation could not have occurred through cross-contamination in a laboratory since the animal and human virus isolations and sequencing were conducted in different locations. Hemagglutination-inhibition (HI) and virus neutralization (VN) assays of acute- and convalescent-phase (11 and 45 days after the acute-phase sample) sera did not show evidence of seroconversion against the patient's own isolate, A/Ontario/RV1273/05 (HI titer = 8 and VN titer = 16 on all 3 test dates). Thus, although this farm worker had a febrile respiratory illness and no other etiologic agent was identified, we cannot prove that he was actively infected with the triple reassortant virus; he may have simply been harboring the virus in his nasal passages. Nonetheless, this isolation shows that agricultural workers may be exposed to influenza viruses from livestock.

In summary, this report describes the emergence and rapid spread since January 2005 of reassortant H3N2 influenza A viruses among pigs and turkeys across Canada and isolation of a related virus from the nasal passages of a farm worker in Ontario. The 4 swine isolates chosen for our analyses provide a sampling of viruses from British Columbia to Ontario, but clinical reports indicate that the outbreak of ILI in pigs was much more extensive than this limited number of isolates might suggest. For example, H3N2 virus infections were confirmed on 22 swine farms in Ontario between late April and early July 2005. Likewise, additional infections of turkeys with H3 viruses in 2005 were reported in British Columbia (on a farm that was near a swine farm where H3 virus was detected [13]) and in multiple flocks in Manitoba (A. Hamel and G. Nayar, pers. comm.). When this Canadian epizootic is considered together with the extensive spread of genotypically similar H3N2 and H1N2 viruses in pigs and turkeys seen in the United States since 1998, we see that viruses with this human/classical swine/avian triple reassortant genotype can efficiently infect both pigs and turkeys.

Behold, happy is the man whom God correcteth: therefore despise not thou the chastening of the Almighty: For he maketh sore, and bindeth up: he woundeth, and his hands make whole ; He shall deliver thee in six troubles: yea, in seven there shall no evil touch thee. - Job 5

Offline TahoeBlue

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It is interesting that when the CDC does re-assortment experiments then a short time later we have an outbreak of something new...

CDC to mix avian, human flu viruses in pandemic study

surprise: http://www.cidrap.umn.edu/cidrap/content/influenza/panflu/news/jan1404hybrids.html
CDC to mix avian, human flu viruses in pandemic study
Jan 14, 2004 (CIDRAP News)

The Centers for Disease Control and Prevention (CDC) will soon launch experiments designed to combine the H5N1 virus and human flu viruses and then see how the resulting hybrids affect animals. The goal is to assess the chances that such a "reassortant" virus will emerge and how dangerous it might be.

CDC officials confirmed the plans for the research as described recently in media reports, particularly in a Canadian Press (CP) story.

Two ways to make hybrids
The plans call for trying two methods to create hybrid viruses, CDC spokesman David Daigle told CIDRAP News via e-mail. One is to infect cells in a laboratory tissue culture with H5N1 and human flu viruses at the same time and then watch to see if they mix. For the human virus, investigators will use A (H3N2), the strain that has caused most human flu cases in recent years, according to the CP report.

Two ways to make hybrids
The plans call for trying two methods to create hybrid viruses, CDC spokesman David Daigle told CIDRAP News via e-mail. One is to infect cells in a laboratory tissue culture with H5N1 and human flu viruses at the same time and then watch to see if they mix. For the human virus, investigators will use A (H3N2), the strain that has caused most human flu cases in recent years, according to the CP report.

The other method is reverse genetics—assembling a new virus with sets of genes from the H5N1 and H3N2 viruses. Reverse genetics has already been used to create H5N1 candidate vaccines in several laboratories, according to Daigle. The National Institutes of Health (NIH) said recently it would soon launch a clinical trial of one of those vaccines.
...
Safety precautions
Because of the obvious risks in creating viruses with the potential to spark a pandemic, the work will be done in a biosafety level 3 (BSL-3) laboratory at the CDC in Atlanta, Daigle told CIDRAP News.
...
BSL-3 is the second highest level of laboratory biosecurity. It is used for work with pathogens that may cause serious or potentially lethal disease if inhaled, such as tuberculosis or St. Louis encephalitis, according to the CDC.

It's been done before
The upcoming experiments will not break entirely new ground for the CDC, the CP story revealed. The agency already has made hybrid viruses with H5N1 samples isolated from patients in Hong Kong in 1997, when the virus first caused human disease.

The results of that research have not yet been published, and the CDC has said little about them. In the CP report, Dr. Nancy Cox, head of the CDC's influenza branch, commented only, "Some gene combinations could be produced and others could not."

Daigle added little to that. He said, "The reassortment work with the 1997 isolate was intermittently interrupted with SARS [severe acute respiratory syndrome] and then the 2004 H5N1 outbreak. We are currently concentrating our efforts on understanding the pathogenicity of the 2004 strains (non-reassortants) in mammalian models."
-------------------------

Now compare that with the H3N2 Swine flu outbeaks....

Influenza viruses of the classical H1N1 lineage were the dominant cause of influenza among North American pigs for >60 years (1). However, in 1998, H3N2 viruses emerged and rapidly spread throughout the US swine population (2–4). These were unique triple reassortant genotype viruses, with hemagglutinin (HA), neuraminidase (NA), and RNA polymerase (PB1) genes of human influenza virus lineage; nucleoprotein (NP), matrix (M), and nonstructural (NS) genes of classical swine virus lineage; and RNA polymerase (PA and PB2) genes of North American avian virus lineage.
....

In October 2004, a 1,000-head swine farm in Minnesota experienced a severe respiratory disease outbreak in 14-week-old pigs, which was characterized by coughing and increased mortality. The morbidity was approximately 80%, and the accumulated mortality reached 5% during the episode. Normal death loss in the index farm was less than 1% prior to the outbreak. Tissues from two dead pigs were submitted to the Veterinary Diagnostic Laboratory at the University of Minnesota for respiratory-disease diagnostic tests.
...

This suggests that A/Swine/Minnesota/00395/2004 H3N1 influenza virus is a reassortant containing genes from triple-reassortant H3N2 and contemporary H1N1 SIVs.
The clinical implications of this reassortant remain to be determined.
..

The recovery of an H3N1 subtype is further evidence of reassortment and antigenic shift in SIVs, justifying ongoing surveillance of animal populations for influenza A viruses that could represent a direct health threat, not only to swine populations, but also to humans.

.....
However, beginning in approximately January 2005, H3N2 influenza viruses swept rapidly across Canada. We describe the genetic characterization of reassortant H3N2 viruses from pigs, turkeys, and a swine farm worker in contact with sick pigs during this outbreak.
...

And in Mexico for the first time:

Serologic evidence of human and swine influenza in Mayan persons.(Dispatches)
January 1, 2005
Antibodies against influenza viruses were detected in 115 serum samples from indigenous Mayan persons from Kochol, Yucatan. Seropositivity rates were 26.9% to A/Bayern/7/95, 40.8% to A/Sydney/5/97, 1.7% to A/Swine/ Wisconsin/238/97, and 79.1% to A/Swine/Minnesota/ 593/99.

This report is the first in Mexico of the prevalence of antibodies to swine influenza virus in humans.

It just seems to me as though these recombinants are being created in labs and then released into pig farms......
Behold, happy is the man whom God correcteth: therefore despise not thou the chastening of the Almighty: For he maketh sore, and bindeth up: he woundeth, and his hands make whole ; He shall deliver thee in six troubles: yea, in seven there shall no evil touch thee. - Job 5

Offline TahoeBlue

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Just in Time for a North American - Global Pandemic?

So now we have S-P / Merck  major Animal Health vaccine manufacturer and sanofi pasteur  the number one human vaccine manufacturer and BIRMEX a "shadowy" Mexican govermental company.

Sanofi-aventis invests €100 million in new facility in Mexico

http://www.worldpharmanews.com/content/view/719/30/
Sanofi-aventis invests €100 million in new facility in Mexico
     
Thursday, 12 March 2009 
Sanofi-aventis (EURONEXT: SAN and NYSE: SNY), has announced the signing of an agreement with the Mexican authorities to build a € 100 million facility to manufacture influenza vaccine in Mexico. The announcement was made during a ceremony attended by Felipe Calderon, President of Mexico, and Nicolas Sarkozy, President of France, who was in Mexico City for a State visit.


This facility will be built and operated by sanofi pasteur, the vaccines division of sanofi-aventis Group, which was represented at the ceremony by Chris Viehbacher, Chief Executive Officer of sanofiaventis.

"By building this new facility, sanofi-aventis is proud to contribute to the strengthening of Mexico's health infrastructure and is eager to support Mexico's exemplary commitment to public health through influenza immunization and pandemic readiness", said Chris Viehbacher. "This investment illustrates sanofi-aventis' local approach to global health. This facility will benefit public health in Mexico and the Latin American region, in the context of influenza pandemic preparedness."

The agreement was signed by Birmex’ (Laboratorio de Biológicos y Reactivos de México) and sanofi-aventis' representatives in the presence of Dr. José Ángel Córdova Villalobos, Minister of Health of Mexico.
 
The new influenza vaccine plant will be built in Ocoyoacac, where sanofi-aventis already operates a facility. The plant will be designed to switch to pandemic vaccine manufacturing if a human influenza pandemic is declared and a pandemic influenza strain is identified by the World Health Organization (WHO).

As the world leader in research, development and manufacturing of influenza vaccines, sanofi pasteur is working to develop new and improved influenza vaccines to save lives and is actively involved in pandemic preparedness. Over the last five years, sanofi pasteur has been consistently investing in major expansions of its influenza vaccine production capacity in the United States, France, China, and now Mexico. With the production of more than 170 million doses of seasonal influenza vaccine in 2008, sanofi pasteur confirmed its global influenza vaccine market leadership.

Seasonal influenza overview
Influenza is a disease caused by a highly infectious virus that spreads easily from person to person, primarily when an infected individual coughs or sneezes. According to the World Health Organization (WHO), the average global burden of inter-pandemic influenza may be on the order of 1 billion cases per year, leading to 300,000-500,000 deaths worldwide. In temperate climate zones, seasonal epidemics typically begin in the late Fall and peak in mid-winter, infecting about 5-15% of the population each season, while In tropical zones the virus can be isolated year-round. The disease can affect all age groups, but rates of infections are highest among young children who spread the virus and are a potential source of infection in older age cohorts, whereas rates of serious illness, complications and death are highest in persons aged 65 years and older, as well as in persons with chronic cardiac or respiratory conditions. The efficacy of vaccination in reducing the burden of the disease, as well as the economic burden of treating influenza, is well established.

Pandemic Influenza Overview
Influenza is a disease caused by a highly infectious virus that spreads easily from person to person, primarily when an infected individual coughs or sneezes. An influenza pandemic is a global epidemic of an especially virulent virus, newly infectious for humans, and for which there is no preexisting immunity. This is why pandemic strains have such potential to cause severe morbidity and mortality. In an attempt to minimize the impact of a pandemic, many countries are developing national and transnational plans against a possible influenza pandemic situation. For more information on sanofi pasteur and pandemic preparedness, please visit http://pandemic.influenza.com.

About sanofi-aventis
Sanofi-aventis, a leading global pharmaceutical company, discovers, develops and distributes therapeutic solutions to improve the lives of everyone. Sanofi-aventis is listed in Paris (EURONEXT: SAN) and in New York (NYSE: SNY).

Sanofi pasteur, the vaccines division of sanofi-aventis Group, provided more than 1.6 billion doses of vaccine in 2008, making it possible to immunize more than 500 million people across the globe. A world leader in the vaccine industry, sanofi pasteur offers the broadest range of vaccines protecting against 20 infectious diseases. The company's heritage, to create vaccines that protect life, dates back more than a century. Sanofi Pasteur is the largest company entirely dedicated to vaccines. Every day, the company invests more than EUR1 million in research and development. For more information, please visit: www.sanofipasteur.com or www.sanofipasteur.us.

BirMex - http://www.birmex.gob.mx/

http://translate.google.com/translate?hl=en&sl=es&u=http://www.birmex.gob.mx/&ei=LPjzSb-XFOCblQeZv7XRDA&sa=X&oi=translate&resnum=1&ct=result&prev=/search%3Fq%3DBirmex%26hl%3Den%26sa%3DG

Biological Laboratories Reagents and Mexico, SA de CV (Birmex) is a company owned by the Federal Government of Mexico that develops, produces and sells imported vaccines, sera and heterologous clinical diagnostic products.

To meet the demand of the Mexican market, Birmex also sells vaccines, immunoglobulins and diagnostic products manufactured by other companies.

Faced with the challenges of the future, Birmex is developing new vaccines  with modern technology to complement its service to its customers.
Behold, happy is the man whom God correcteth: therefore despise not thou the chastening of the Almighty: For he maketh sore, and bindeth up: he woundeth, and his hands make whole ; He shall deliver thee in six troubles: yea, in seven there shall no evil touch thee. - Job 5

Offline TahoeBlue

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Roche in Mexico....

http://www.manattjones.com/newsletters/newsbrief/20070930.htm

Roche Inaugurates Facility In Toluca
September 26, 2007

The Mexican subsidiary of Swiss Pharmaceutical company Roche, Grupo Roche Syntex de Mexico, inaugurated a USD 60 million facility to produce high-powered drugs to treat cancer, transplants and osteoporosis among other diseases. The plant has the capacity to manufacture 250 tons of medicine a year, of which 90% will be exported to the U.S., Europe, Asia and the rest of the world; 7% of the production will be distributed between Mexico and Latin America. The Toluca facility is one of three Roche facilities in the world to produce high-powered drugs.

http://www.hindu.com/2005/11/09/stories/2005110907791700.htm

DRL to acquire Roche's Mexico business
Special Correspondent
Nov 09, 2005

HYDERABAD: Dr. Reddy's Laboratories has entered into a definitive agreement to acquire Roche's active pharmaceutical ingredient (API) business at the latter's state-of-the-art manufacturing site in Cuernavaca, Mexico. The acquisition includes all employees and business supply contracts and the total investment is about $59 million
, including working capital. The acquisition is expected to be completed by the end of December.

The deal involves the manufacture and sale of APIs, including intermediates to Roche and other Innovator Companies. The product portfolio now comprises about 18 products, including mature APIs and a range of intermediates and steroids.
Behold, happy is the man whom God correcteth: therefore despise not thou the chastening of the Almighty: For he maketh sore, and bindeth up: he woundeth, and his hands make whole ; He shall deliver thee in six troubles: yea, in seven there shall no evil touch thee. - Job 5

Offline TahoeBlue

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GlaxoSmithKline is there too....

http://goliath.ecnext.com/coms2/product-compint-0000504747-page.html

Company Profile
Updated: 27-MAR-09
GlaxoSmithKline de Mexico S.A. de C.V.
International Private company
Mexico-Xochimilco 4900, Col. San Lorenzo Huipulco, Delegacion Tlalpan, Mexico DF,  14370, Mexico
()52 55 5483 8398, 52 55 5483 8400 fax, http://www.gsk.com.mx
Primary SIC: Pharmaceutical Preparations, Primary NAICS: Pharmaceutical Preparation Manufacturing
Description: Manufacturing: Manufacture of pharmaceuticals products, cosmetics; importer and exporter

http://www.medicalnewstoday.com/articles/18718.php
GSK's Global Launch with Rotarix(TM) starts in Mexico (for rotavirus)
Main Category: Pediatrics / Children's Health
Article Date: 09 Jan 2005 - 0:00 PDT

GlaxoSmithKline (GSK) announced the launch of Rotarix(TM) in Mexico representing the first concrete step for GSK in providing a safe and effective vaccine to prevent rotavirus globally.

Rotavirus infection is the leading cause of severe diarrhea and vomiting in infants and young children between 6 and 36 months worldwide. If untreated, the virus can rapidly kill, as the sickest children become dehydrated from 10 to 20 episodes of diarrhea in a single day. Globally, rotavirus infections account for approximately 138 million cases of infantile gastroenteritis each year and are responsible for approximately 440,000 deaths per year globally -- one child a minute.

As part of GSK Biologicals novel and unique global strategy to develop and deliver vaccines first to those with the greatest medical need, Rotarix(TM) obtained licensure on July 12th 2004 from the Mexican regulatory authorities.

Rotarix(TM) will be launched in many other Latin American countries in the course of 2005 and will start also to be launched in Asia Pacific. Rotarix(TM) has already been filed in more than 20 countries worldwide.

"GSK has a solid track record of providing vaccines globally for more than 20 years and is constantly developing novel and unique approaches to ensure new vaccines get to those areas of the world who need them most as fast as possible", said Jean Stiphenne, President and General Manager of GSK Biologicals. "In the case of Rotarix(TM), we focussed our clinical and regulatory strategy first on countries where the medical need for a rotavirus vaccine was amongst one of the highest in the world."

GlaxoSmithKline Biologicals

GlaxoSmithKline Biologicals (GSK Biologicals), one of the world's leading vaccine manufacturers, is located in Rixensart, Belgium, which is the center of all GlaxoSmithKline's activities in the field of vaccine research, development and production. GSK Biologicals employs more than 1000 research scientists, who are devoted to discovering new vaccines and developing more cost-effective and convenient combination products to prevent infections that cause serious medical problems worldwide.

In 2003, GSK Biologicals distributed more than 850 million doses of vaccines to 152 countries in both the developed and the developing world - an average of 27 doses per second. Of those vaccine doses, approximately 85 million were doses of combination pediatric vaccines, which protect the world's children against a minimum of three -- and as many as six - diseases in one vaccine. For more information, visit GlaxoSmithKline's vaccine websites at http://www.gsk-bio.com and http://www.worldwidevaccines.com (for both healthcare professionals and general public).

GlaxoSmithKline (GSK) -- one of the world's leading research-based pharmaceutical and healthcare companies -- is committed to improving the quality of human life by enabling people to do more, feel better and live longer.


http://www.drugresearcher.com/Research-management/GSK-purchases-Wyeth-s-vaccine-facility

GSK purchases Wyeth's vaccine facility
By Wai Lang Chu, 02-Sep-2005

Britiain's largest drugsmaker, GlaxoSmithKline, announced it is to expand its ability to increase vaccines supplies by acquiring a vaccine research and production facility from rivals Wyeth.

This acquisition adds to the company's growing vaccines presence following GSK's May's purchase of Corixa Corporation, a developer of vaccine adjuvants that increase immune response.

"We are working hand-in-hand with government officials to help meet public health needs by expanding our capabilities as a reliable supplier of vaccines for the US," said JP Garnier, chief executive officer of GlaxoSmithKline.

The 90-acre manufacturing site, located in Marietta, Pennsylvania, which Wyeth closed in December, will be used to help develop future vaccines for GlaxoSmithKline. Terms of the acquisition were kept confidential

The site will focus on the development and production of tissue culture technology that will be used for seasonal and pandemic flu vaccines.

GSK expects to use the site's freeze-drying capabilities to enhance the shelf life and stability of a number of the company's vaccines.

In May, the company filed an application with the Food and Drug Administration (FDA) to market its flu vaccine Fluarix in the US in time for the upcoming flu season.

Glaxo's flu vaccine is produced in Dresden, Germany. On Wednesday, the company won FDA approval to sell flu shots in the United States for the first time. It expects to provide about 8 million doses for the US.

The purchase could be seen as an attempt to fill the gap in future supplies of flu jabs, which saw vaccine suppliers struggling to keep up with demand.

Last year, problems at the Liverpool plant of the US biotech firm Chiron led to a global shortage of vaccine.

GSK's $300 million purchase of Corixa, which makes a component of the cervical cancer vaccine Cervarix, and this latest deal, serves as an indication of the groups shift in focus to vaccine production and manufacturing.

In the next five years, GSK hopes to launch five major new vaccines in some countries: Cervarix, an HPV vaccine targeting cervical cancer; Rotarix, a vaccine against rotavirus already approved in 13 countries including Mexico; a vaccine to prevent pneumococcal disease; an improved flu vaccine for the elderly; and a meningitis combination vaccine for infants in the US.
Behold, happy is the man whom God correcteth: therefore despise not thou the chastening of the Almighty: For he maketh sore, and bindeth up: he woundeth, and his hands make whole ; He shall deliver thee in six troubles: yea, in seven there shall no evil touch thee. - Job 5

Offline David Rothscum

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http://www.newscientist.com/article/dn4810-bird-flu-vaccination-could-lead-to-new-strains.html

 Bird flu vaccination could lead to new strains

    * 19:00 24 March 2004 by Debora MacKenzie

Vaccinating chickens may be the only way out of the bird flu nightmare in Asia. But it could also lead to the evolution of new strains, the latest research shows, increasing the risk of a human pandemic.

Only intensive surveillance can stop this happening, but experts say the countries affected do not have the necessary systems in place.

Last week China declared its bird flu outbreaks had ended. Health officials are vaccinating millions of the birds that escaped slaughter. Indonesia is also vaccinating, and other Asian countries hit by the H5N1 bird flu are considering the same strategy.

But the H5N1 virus is almost certainly still circulating among the vaccinated birds, and the fear is that in this abnormal setting it may evolve into a form that is not only fatal to people, like the current one, but can also spread from person to person.

Research in Mexico has shown for the first time that under these conditions bird flu evolves at an unprecedented rate, with unpredictable consequences.
Silent epidemics

Veterinary scientists usually prefer to control livestock epidemics by destroying sick and exposed animals, instead of vaccinating.

The reason is that vaccines, especially flu ones, are not 100 per cent effective. While they prevent animals falling ill, low numbers of viruses can still replicate inside their bodies and spread from animal to animal. Such "silent epidemics" are very hard to spot, but can cause new outbreaks if unvaccinated animals are exposed or if vaccination ends.

But with H5N1 bird flu now affecting a huge area of Asia, vaccination could help end the outbreaks more quickly. Fewer flocks destroyed would leave fewer small-scale poultry farmers destitute. "They really have few choices now," says Ilaria Capua of the World Organisation for Animal Health reference lab for bird flu in Legnaro in Italy.

There is a precedent ­ but it is a worrying one. In 1995 Mexico stopped an outbreak of severe H5N2 flu by vaccinating chickens. But the virus is still circulating silently, and Mexico is still vaccinating.

Normally the bird flu virus changes little in chickens, because it rarely persists long enough, says David Suarez of the US Department of Agriculture's poultry research lab in Georgia. But in Mexico the virus has been exposed to vaccinated chickens for years and this has encouraged new forms to evolve.
Major differences

In a report that will appear in the Journal of Virology, Suarez's team reveals that "major antigenic differences" have been found in the bird flu viruses isolated from vaccinated chickens in Mexico since 1995. It is increasingly different to the vaccine strain, which means that infected birds will shed more of the virus and spread the infection more readily.

The H5N1 virus circulating in vaccinated chickens in Asia is likely to evolve the same way. There has already been speculation that vaccination programmes in China may have led to greater genetic diversity in the virus over the past two years, and perhaps even contributed to the emergence of the current strain ( New Scientist, 28 January).

It is possible, however, to eradicate wild virus like H5N1 from vaccinated flocks. The key is to detect and destroy silent infections. The low-tech way of doing this is to place unvaccinated birds next to vaccinated flocks.

If any flu is circulating, these "sentinel" birds will develop obvious symptoms. The weakness of this system, says Capua, is that farmers who want to save their flocks from destruction can cheat by replacing any sick birds.
Marker vaccine

The high-tech method is to use a marker vaccine that elicits the production of a different set of antibodies to the wild virus. Antibody tests can then distinguish between infected birds and those that have simply been vaccinated. In 2002 Italy became the first country to eradicate bird flu using a marker vaccine and regular testing.

The surveillance part is vital, Capua says. "The vaccine used without this monitoring can have a boomerang effect, and become a tool to spread the virus, not control it."

Richard Webby, a leading flu expert at St Jude Children's Research Hospital in Memphis, Tennessee, agrees. "The key to using vaccination successfully is strong surveillance, with a vaccination versus infection marker," he says.

China does at least have the right vaccines. Its agriculture ministry announced last week that it is launching two marker vaccines. But thousands of vaccinated chickens must still be tested, and infected flocks destroyed, to eliminate the virus.

Yet such surveillance systems will be a tall order for the Asian countries that are vaccinating or plan to. Joseph Domenech, head of animal health at the UN Food and Agriculture Organization, says that Indonesia, which is vaccinating chickens, does not have adequate controls. "In China, we just do not know," he says, while Vietnam has not revealed its plans.

If you would like to reuse any content from New Scientist, either in print or online, please contact the syndication department first for permission. New Scientist does not own rights to photos, but there are a variety of licensing options available for use of articles and graphics we own the copyright to.

Offline TahoeBlue

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Baxter in Mexico...

http://www.baxter.com/about_baxter/news_room/news_releases/2008/12_19_08_industryweek.html

Baxter Plant in Mexico Named Among IndustryWeek's Top 10 Best Plants

DEERFIELD, Ill., December 19, 2008 — Baxter’s manufacturing plant in Cuernavaca, Mexico has been named one of the 10 Best Plants in North America for 2008 by IndustryWeek magazine. Winners of the competition were selected based on key performance metrics, as well as dedication to continually improving people and processes.

"Baxter is honored to receive this important recognition from IndustryWeek," said Alejandro Ochoa Ortiz, plant manager. "This recognition represents our strong commitment to excellence in the management and operation of the Cuernavaca facility."

The Baxter Mexico S.A. de C.V facility was the only Mexican manufacturing plant chosen among the IndustryWeek winners, and is considered a pacesetter in operational strategy, production practices and performance. Baxter has placed a strong emphasis on "lean" manufacturing principles that have improved efficiency at the plant. In the past three years, this has generated significant cost savings, improvements in manufacturing processes, and fewer lost workdays. As a result, productivity has improved by nearly 30 percent.

"This is a facility that embraces change to better serve our customers," said Ortiz. "As a healthcare company, we are privileged to work in an industry where the work we do benefits so many. What makes our business so rewarding also presents our greatest challenge: ensuring the safety and efficacy of our products, which are used millions of times each day by patients worldwide to treat critical, life-threatening conditions."

Baxter’s Cuernavaca facility manufactures renal products and intravenous solutions and employs approximately 1,300 employees. The plant has received the 2008 "Clean Industry" Award; the 2007 Shingo Prize; the 2008 100 Best Companies to Work for in Mexico Award; and the 2008 35 Best Companies for Working Women in Mexico Award.

Winners of the IndustryWeek competition will be recognized at the annual IW Best Plants Conference, which will be held April 27-29, 2009 in Nashville. For more
 
 About Baxter

Baxter S.A. de C.V. is a subsidiary of Baxter International Inc. Baxter assists healthcare professionals and their patients with treatment of complex medical conditions, including hemophilia, immune disorders, infectious diseases, kidney disease, trauma and other indications. The company applies its expertise in medical devices, pharmaceuticals and biotechnology to make a meaningful difference in patients’ lives.
http://goliath.ecnext.com/coms2/product-compint-0000506054-page.html
 
Company Profile
Updated: 11-MAR-09
Baxter S.A. de C.V.
International Private company
Insurgentes Sur 1196, Colonia del Valle, Mexico DF,  03200, Mexico
()52 55 9126 5000, 52 55 5335 1005 fax, http://www.baxter.com.mx
Primary SIC: Surgical And Medical Instruments, Primary NAICS: Surgical and Medical Instrument Manufacturing
Description: Manufacturing: Manufacture of products used and consumed primarily in the health care field including blood collection bags

http://www.chicagotribune.com/business/chi-baxter-swine-flu-27-apr27,0,3579388.story
Swine flu: Baxter seeks swine flu sample to begin work on vaccine
Deerfield-based Baxter has a speedier way to make vaccines than old method
By Bruce Japsen | Tribune reporter
April 27, 2009

By Bruce Japsen | Tribune reporter
April 27, 2009

With world health officials worried about the global outbreak of another deadly virus, Deerfield-based Baxter International Inc. once again finds itself involved in the action.

Baxter confirmed over the weekend that it is working with the World Health Organization on a potential vaccine to curb the deadly swine flu virus that is blamed for scores of deaths in Mexico and has emerged as a threat in the U.S.

Baxter, which has an emerging vaccine business, has worked with the U.S. and foreign countries in the past to develop vaccines for the H5N1 virus commonly known as bird flu.

Baxter has a cell-based technology that allows the company to produce vaccines more rapidly in the event of a pandemic than a decades-old method that uses eggs and can take weeks or months longer. Although the egg-based method has produced safe and effective vaccines, analysts say Baxter's method can cut production times in half compared with the older process.

"Upon learning about the swine flu outbreak in Mexico, Baxter requested a virus sample from WHO to do laboratory testing for potentially developing an experimental vaccine," company spokesman Christopher Bona told the Tribune.

In the past, Baxter has developed vaccines and worked with countries to stockpile vaccines even while they undergo experimental testing.

The idea behind the government stockpiles, in the case of the bird flu, for example, is to prepare against outbreak.

As of Sunday, Baxter would not say whether the U.S. or other countries have contacted the company to develop a stockpile against swine flu. Other companies, too, develop vaccines and have been used to stockpile vaccines.

The effort to ensure a safe vaccine supply and an adequate number of manufacturers has taken on greater importance in recent years.

Three years ago, for example, the Bush administration awarded about $1 billion to vaccine makers as a way to increase and speed production, particularly after the spread of bird flu.

Several vaccine makers, including Baxter, GlaxoSmithKline and others, were awarded multimillion-dollar contracts.

Baxter, working with another company, was awarded a five-year contract to develop both seasonal and pandemic vaccines using its cell-based technology, according to terms of the deal disclosed in May 2006.

Over the years, Baxter has worked with governments around the world to develop and produce vaccines to protect against infectious disease or potential threats from bioterrorism.

In the wake of the terrorist attacks on Sept. 11, 2001, Baxter worked with British biotech company Acambis to supply stockpiles of a smallpox vaccine.

In 2003, Baxter was awarded a U.S. contract to develop and produce a vaccine against severe acute respiratory syndrome (SARS) for use by the National Institutes of Health in early human clinical trials.

And in 2005, Baxter worked with another company to develop a "plasma-based therapeutic targeted for use in individuals who may be exposed to nerve gas poisons," the company said at the time.

Because it's so early in the swine flu vaccine development process, Baxter would not estimate when a vaccine might be ready.

[email protected]

http://www.legitgov.org/baxter_flu_vaccine_260409.html

Baxter working on vaccine to stop swine flu, though admitted sending live pandemic flu viruses to subcontractor
By Lori Price, www.legitgov.org 26 Apr 2009


The OMFG moment of the century: Illinois-based Baxter working on vaccine to 'stop' swine flu outbreak in Mexico 25 Apr 2009 Specialty drug maker Baxter International Inc. will work with the World Health Organization to develop a vaccine that could stem [foment] an outbreak of a deadly swine flu strain in Mexico. Baxter spokesman Christopher Bona said Saturday that the Deerfield, Ill.-based company has asked the WHO for a sample of the flu strain. He says Baxter has patented technology that allows the company to develop vaccines in half the time it usually takes -- about 13 weeks instead of 26. [Is Baxter International taking a page from the Blackwater playbook? Just as Blackwater/Xe keep on killing to justify their multi-billion dollar contracts to provide 'security' in Iraq and Afghanistan, Baxter International is poised to make *billions* to vaccinate people against their pandemic.]

Are you ready? Wait for it...

http://timesofindia.indiatimes.com/Health--Science/Science/Virus-mix-up-by-lab-could-have-resulted-in-pandemic/articleshow/4230882.cms
Virus mix-up by lab could have resulted in pandemic [Uh, it apparently f*cking *did.*] 06 Mar 2009 It's emerged that virulent H5N1 bird flu was sent out by accident from an Austrian lab [the Austrian branch of US vaccine company, Baxter] last year and given to ferrets in the Czech Republic before anyone realised. As well as the risk of it escaping into the wild, the H5N1 got mixed with a human strain, which might have spawned a hybrid that could unleash a pandemic.

http://www.lifegen.de/newsip/shownews.php4?getnews=2009-02-25-5123
'This was infected with a bird flu virus.' Viral Pandemic H5N1 flu threat: Illinois-based Baxter contaminates European labs by error 25 Feb 2009 According to the scientific network PROMED, Baxter International Inc. in Austria "unintentionally contaminated samples with the bird flu virus that were used in laboratories in 3 neighboring countries, raising concern about the potential spread of the deadly disease". As PROMED reports, the contamination has been discovered when ferrets at a laboratory in the Czech Republic died after being inoculated with vaccine made from the samples early this month. "The material came from Deerfield, Illinois-based Baxter, which reported the incident to the Austrian Ministry of Health, Sigrid Rosenberger, a ministry spokeswoman, said today in a telephone interview", the network-alert-system is quoting. "This was infected with a bird flu virus," Rosenberger said. "There were some people from the company who handled it."

http://www.legitgov.org/baxter_sends_live_avian_flu_viruses_270209.html
'That mixing process, called reassortment, is one of two ways pandemic viruses are created.'

Baxter admits sending live avian flu viruses to subcontractor --People familiar with biosecurity rules are dismayed by evidence that human H3N2 and avian H5N1 viruses somehow co-mingled [!] in the Orth-Donau facility. 27 Feb 2009 The company that released contaminated flu virus material from a plant in Austria confirmed Friday that the experimental product contained live H5N1 avian flu viruses. And an official of the World Health Organization's European operation said the body is closely monitoring the investigation into the events that took place at Baxter International's research facility in Orth-Donau, Austria. [Source: The Canadian Press
...
Behold, happy is the man whom God correcteth: therefore despise not thou the chastening of the Almighty: For he maketh sore, and bindeth up: he woundeth, and his hands make whole ; He shall deliver thee in six troubles: yea, in seven there shall no evil touch thee. - Job 5

Offline TahoeBlue

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http://www.newscientist.com/article/dn4810-bird-flu-vaccination-could-lead-to-new-strains.html

 Bird flu vaccination could lead to new strains
    * 19:00 24 March 2004 by Debora MacKenzie

Vaccinating chickens may be the only way out of the bird flu nightmare in Asia. But it could also lead to the evolution of new strains, the latest research shows, increasing the risk of a human pandemic.
...

Or, One could also say:

Vaccinating Pigs may be the only way out of the Swine/Avian/Human flu nightmare in Mexico.
But it could also lead to the evolution of new strains, the latest research shows, increasing the risk of a human pandemic.

Oh, but we are already vaccinating pigs....  increasing the risk of a human pandemic
Behold, happy is the man whom God correcteth: therefore despise not thou the chastening of the Almighty: For he maketh sore, and bindeth up: he woundeth, and his hands make whole ; He shall deliver thee in six troubles: yea, in seven there shall no evil touch thee. - Job 5

Offline powderfinger

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Wow. This is some great research! Thank you. I can't wait to dig in and assimilate it. Keep it coming!

Offline rawiron1

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CDC to mix avian, human flu viruses...
« Reply #19 on: April 28, 2009, 10:10:36 am »
http://www.cidrap.umn.edu/cidrap/content/influenza/panflu/news/jan1404hybrids.html


CDC to mix avian, human flu viruses in pandemic study

Robert Roos * News Editor

Jan 14, 2004 (CIDRAP News) – One of the worst fears of infectious disease experts is that the H5N1 avian influenza virus now circulating in parts of Asia will combine with a human-adapted flu virus to create a deadly new flu virus that could spread around the world.

That could happen, scientists predict, if someone who is already infected with an ordinary flu virus contracts the avian virus at the same time. The avian virus has already caused at least 48 confirmed human illness cases in Asia, of which 35 have been fatal. The virus has shown little ability to spread from person to person, but the fear is that a hybrid could combine the killing power of the avian virus with the transmissibility of human flu viruses.

Now, rather than waiting to see if nature spawns such a hybrid, US scientists are planning to try to breed one themselves—in the name of preparedness.

The Centers for Disease Control and Prevention (CDC) will soon launch experiments designed to combine the H5N1 virus and human flu viruses and then see how the resulting hybrids affect animals. The goal is to assess the chances that such a "reassortant" virus will emerge and how dangerous it might be.

CDC officials confirmed the plans for the research as described recently in media reports, particularly in a Canadian Press (CP) story.

Two ways to make hybrids
The plans call for trying two methods to create hybrid viruses, CDC spokesman David Daigle told CIDRAP News via e-mail. One is to infect cells in a laboratory tissue culture with H5N1 and human flu viruses at the same time and then watch to see if they mix. For the human virus, investigators will use A (H3N2), the strain that has caused most human flu cases in recent years, according to the CP report.

The other method is reverse genetics—assembling a new virus with sets of genes from the H5N1 and H3N2 viruses. Reverse genetics has already been used to create H5N1 candidate vaccines in several laboratories, according to Daigle. The National Institutes of Health (NIH) said recently it would soon launch a clinical trial of one of those vaccines.

Of the two methods, the co-infection approach was described as slower and more laborious, though closer to what happens in nature.

Any viable viruses that emerge from these processes will be seeded into animals that are considered good models for testing how flu viruses behave in humans, according to Daigle. The aim will be to observe whether the animals get sick and whether infected animals can infect others.

The World Health Organization (WHO) has been "pleading" for laboratories to do this research, because it could provide some evidence to back up the agency's warnings about the risk of a flu pandemic, according to the CP report.

Klaus Stohr, head of the WHO's global influenza program, was quoted as saying that if none of the hybrids caused disease, the agency might be inclined to dial down its level of concern. But if the experiments produce highly transmissible and pathogenic viruses, the agency will be more worried, he said.

Safety precautions
Because of the obvious risks in creating viruses with the potential to spark a pandemic, the work will be done in a biosafety level 3 (BSL-3) laboratory at the CDC in Atlanta, Daigle told CIDRAP News.

"We recognize that there is concern by some over this type of work. This concern may be heightened by reports of recent lab exposures in other lab facilities," he said. "But CDC has an incredible record in lab safety and is taking very strict precautions."

Daigle said the US Department of Agriculture requires that highly pathogenic avian influenza (HPAI) viruses be treated as "Select Agents" and that research on them must be done in BSL-3 labs with "enhancements." These include "special provisions to protect both laboratory workers and the environment."

BSL-3 is the second highest level of laboratory biosecurity. It is used for work with pathogens that may cause serious or potentially lethal disease if inhaled, such as tuberculosis or St. Louis encephalitis, according to the CDC.

CDC experiments with HPAI viruses have to pass reviews by the agency's Institutional Biosafety Committee and Animal Care and Use Committee, Daigle said. The facilities involved are inspected by the USDA and the CDC's Office of Safety and Health, and staff members who work with Select Agents require special clearance.

It's been done before
The upcoming experiments will not break entirely new ground for the CDC, the CP story revealed. The agency already has made hybrid viruses with H5N1 samples isolated from patients in Hong Kong in 1997, when the virus first caused human disease.

The results of that research have not yet been published, and the CDC has said little about them. In the CP report, Dr. Nancy Cox, head of the CDC's influenza branch, commented only, "Some gene combinations could be produced and others could not."

Daigle added little to that. He said, "The reassortment work with the 1997 isolate was intermittently interrupted with SARS [severe acute respiratory syndrome] and then the 2004 H5N1 outbreak. We are currently concentrating our efforts on understanding the pathogenicity of the 2004 strains (non-reassortants) in mammalian models."

He said the CDC hopes to prepare a report on that research "in the near future."

See also:

CDC information on biosafety levels

http://www.cdc.gov/od/ohs/symp5/jyrtext.htm
Jason the Fed

Offline Freeski

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You say it weakens as it mutates, but can't it also strengthen itself as it picks up new traits, like in the direction of a superbug?
"He who passively accepts evil is as much involved in it as he who helps to perpetrate it. He who accepts evil without protesting against it is really cooperating with it." Martin Luther King, Jr.

Offline TahoeBlue

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You say it weakens as it mutates, but can't it also strengthen itself as it picks up new traits, like in the direction of a superbug?

The question is what is left to replicate.
With the death of the host, the lethal forms no longer have a host to replicate in.
Surviving hosts with the less lethal forms have plenty of other hosts to replicate to.

So over time, less lethal forms overcome the lethal forms. The lethal forms dissappear (fail to replicate to other hosts).

"Superbugs" are almost univerally "created" in labs. Only if the lethal form has a way of continually infecting new hosts will it be observed. Look at the history of Bubonic plague for an example of a real superbug not created in a lab.
Behold, happy is the man whom God correcteth: therefore despise not thou the chastening of the Almighty: For he maketh sore, and bindeth up: he woundeth, and his hands make whole ; He shall deliver thee in six troubles: yea, in seven there shall no evil touch thee. - Job 5

Offline Freeski

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The question is what is left to replicate.
With the death of the host, the lethal forms no longer have a host to replicate in.
Surviving hosts with the less lethal forms have plenty of other hosts to replicate to.

So over time, less lethal forms overcome the lethal forms. The lethal forms dissappear (fail to replicate to other hosts).

Interesting... thanks.
"He who passively accepts evil is as much involved in it as he who helps to perpetrate it. He who accepts evil without protesting against it is really cooperating with it." Martin Luther King, Jr.

Offline TahoeBlue

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Interesting... thanks.

I lived in San Francisco when Aids started. They were dropping left and right. It had all the signs of a BioWeapon. The one's who were initially infected all died.  Those that were infected later for the most part at least survived longer. Now they call it HIV. What we see now is not what I saw going on back in 1978-1982.
Behold, happy is the man whom God correcteth: therefore despise not thou the chastening of the Almighty: For he maketh sore, and bindeth up: he woundeth, and his hands make whole ; He shall deliver thee in six troubles: yea, in seven there shall no evil touch thee. - Job 5

Offline msr

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Tahoe, did people suspect that the government did it back then? I mean created aids.


Offline TahoeBlue

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Tahoe, did people suspect that the government did it back then? I mean created aids.
It took a year or so for people to really suspect it. No one had seen anything like it. Only later when the connection was made to the hepetitus B vaccine given to NY "fire island"  gays (all the gays that received that vaccine got aids and died), did people and doctors suspect. Then also the connection of Dr. Gallo to BW's work for the government. Evidence began to snowball. We're just conspiracy theorists.
Behold, happy is the man whom God correcteth: therefore despise not thou the chastening of the Almighty: For he maketh sore, and bindeth up: he woundeth, and his hands make whole ; He shall deliver thee in six troubles: yea, in seven there shall no evil touch thee. - Job 5

Offline TahoeBlue

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Add to timeline :

Oct 2004 - reconstruction of 1918 Swine Flu

Human Error and Biosafety Laboratories

"The researchers working on the 1918 virus say their work is vital to understand what changes make flu viruses dangerous."

Or one could also say:

"The researchers working on the 1918 virus say their work is vital to understand HOW TO make flu viruses dangerous."

Several teams have added one or more of these genes to modern flu viruses, or plan to – in effect partially recreating the long-vanished pandemic virus.

The researchers also found that people born after 1918 have little or no immunity.

http://www.ace-ej.org/BiolabWeb/Biolabdocs/Klotztestimony.pdf

Human Error and Biosafety Laboratories
(Carelessness, Poor Training, and Poor Judgment)
Testimony of: Lynn C. Klotz, PhD

Scientists Working Group on Chemical and Biological Weapons
Center for Arms Control and Non Proliferation


Today, I wish to address public-health risk from human error in Biosafety-level 3 and 4 laboratories. These errors include accidents from carelessness or inadequate training, or poor judgment. Intensive public-health, scientific and political oversight of biosafety laboratories can reduce this risk.

Dangerous experiments
10:33 21 October 2004
Exclusive from New Scientist Print Edition.

The 1918 flu virus spread across the world in three months and killed at least 40 million people. If it escaped from a lab today, the death toll could be far higher.

“The potential implications of an infected lab worker – and spread beyond the lab – are terrifying,” says D. A. Henderson of the University of Pittsburgh, a leading biosecurity expert.

Yet despite the danger, researchers in the US are working with reconstructed versions of the virus at less than the maximum level of containment. Many other experts are worried about the risks. “All the virologists I have spoken to have concerns,” says Ingegerd Kallings of the Swedish Institute for Infectious Disease Control in Stockholm, who helped set laboratory safety standards for the World Health Organization.

Work on the 1918 flu virus is not the only worry. Some experiments with bird flu have also been criticised as dangerous (New Scientist print edition, 28 February 2004).

Kallings and others are calling for international discussions to resolve the issues related to such work. “It is time for influenza scientists to find a consensus on containment,” she says. John MacKenzie of the University of Queensland in Australia, who investigated how the SARS virus escaped from high-level containment labs in east Asia on three occasions after lab workers became infected, agrees. “A meeting would be beneficial.”

Gene sequencing
The researchers working on the 1918 virus say their work is vital to understand what changes make flu viruses dangerous. So far five of the 1918 flu virus’s eight genes have been sequenced, using fragments retrieved from victims of the pandemic.

Several teams have added one or more of these genes to modern flu viruses, or plan to – in effect partially recreating the long-vanished pandemic virus.

The latest work was done by Yoshihiro Kawaoka at the University of Wisconsin at Madison. His team showed that adding the 1918 gene for the surface protein haemagglutinin to modern viruses made them far deadlier to mice.

The researchers also found that people born after 1918 have little or no immunity.

The team started the work at the highest level of containment, BSL-4, at Canada’s National Microbiology Laboratory in Winnipeg. Then they decided the viruses were safe enough to handle at the next level down, and did the rest of the work across the border in a BSL-3Ag lab in Madison. The main difference between BSL-4 and BSL-3Ag is that precautions to ensure staff do not get infected are less stringent: while BSL-4 involves wearing fully enclosed body suits, those working at BSL-3Ag labs typically have half-suits.

Kawaoka told New Scientist that the decision to move down to BSL-3Ag was taken only after experiments at BSL-4 showed that giving mice the antiviral drug oseltamivir (Tamiflu) in advance prevented them getting sick. This means, he says, that if all lab workers take oseltamivir “they cannot become infected”.

Contradictory results
Yet this assumes that the mouse results apply to humans. And the findings have not been published. In similar experiments, Terrence Tumpey’s team at the US Department of Agriculture’s poultry research lab in Athens, Georgia, got quite different results: they found that mice given oseltamivir still got sick and 1 in 10 died. It is not clear why Kawaoka’s mice fared better.

What is more, all the safety precautions are aimed at preventing escape, not dealing with it should it occur. If any of Kawaoka’s lab workers are exposed to the virus despite all the precautions, and become infected despite taking oseltamivir, the consequences could be disastrous.

“I experienced disbelief…regarding the decision to relocate the reconstructed 1918 influenza strain from a BSL-4 facility to a BSL-3 facility, based on its susceptibility to antiviral medication,” Ronald Voorhees, chief medical officer at the New Mexico Department of Health, wrote on ProMED-mail, an infectious diseases mailing list.

Yet Kawaoka’s decision does comply with the US National Institutes of Health guidelines for BSL-3 agents: those causing “serious or lethal human disease for which preventive or therapeutic interventions may be [its italics] available”. In fact, he is considered unusually cautious. “Kawaoka should be applauded for using BSL-4 at all,” says Richard Webby, a flu researcher at St Jude’s Children’s Hospital in Memphis, Tennessee.

Exposing monkeys
By contrast, the team in Georgia, the first to experiment with genetically engineered 1918 viruses, did all its work at BSL-3Ag. Meanwhile, Michael Katze at the University of Washington at Seattle is planning to expose monkeys to aerosols of 1918-type viruses at BSL-3, a step down from BSL-3Ag.
The recent SARS escapes were from BSL-3 labs.

“We would have to do any such work at BSL-4,” says John Wood of the UK’s National Institute for Biological Standards and Control.

 In the US, the differing standards applied by different groups are due to the fact that experiments on engineered viruses such as the 1918 flu are approved on a case-by-case basis by Institutional Biosafety Committees (IBCs), composed of local scientists and officials. Critics say these are free to interpret the official guidelines in a way that suits them.
“There is no effective national system to ensure consistency, responsibility and good judgement in such research,” says Edward Hammond of the Sunshine Project, a biosecurity pressure group in Austin, Texas. In a review of IBCs published this month, he found that many would not provide minutes of recent meetings as required by law.

He says the IBC that approved the planned 1918 flu study at the University of Washington considered only one scenario that could result in workers being exposed to airborne virus – the dropping of samples. Its solution: lab workers “will be trained to stop breathing”.

http://www.newscientist.com/news/news.jsp?id=ns99994713

Superflu is being brewed in the lab

After the worldwide alarm triggered by 2003's SARS outbreak, it might seem reckless to set about creating a potentially far more devastating virus in the lab. But that is what is being attempted by some researchers, who argue that the dangers of doing nothing are even greater.

We already know that the H5N1 bird flu virus ravaging poultry farms in Asia can be lethal on the rare occasions when it infects people. Now a team is tinkering with its genes to see if it can turn into a strain capable of spreading from human to human.

If they manage this, they will have created a virus that could kill tens of millions if it got out of the lab.

Rodents and monkeys
Some researchers refuse to discuss their plans. But Jacqueline Katz at the US Centers for Disease Control (CDC) in Atlanta, Georgia, told New Scientist her team is already tweaking the genes of the H5N1 bird flu virus that killed several people in Hong Kong in 1997, and those of the human flu virus H3N2.

She is testing the ability of the new viruses to spread by air and cause disease in ferrets, whose susceptibility to flu appears to be remarkably similar to ours.

Albert Osterhaus of Erasmus University in Rotterdam in the Netherlands plans to test altered viruses on rodents and macaque monkeys. Other groups are also considering similar experiments, he says.
Many researchers say experiments like this are needed to answer crucial questions. Why can a few animal flu viruses infect humans? What makes the viruses deadly? And what changes, if any, would enable them to spread from person to person and cause pandemics that might prove far worse than that of 1918? Once we know this, they argue, we will be better prepared for whatever nature throws at us.
Others disagree. It is not clear how much we can learn from such work, they argue. And they point out that it is already possible to create a vaccine by other means. The work is simply too dangerous, they say.

If such work were to show that H5N1 could cause a human pandemic, everything that is happening in Asia would be even more alarming, Osterhaus argues.

If, on the other hand, it failed to transform H5N1 into a highly contagious human virus, we could relax. "It becomes a veterinary health problem, not a public health problem. That would be an
enormous relief."
"I'm getting bombarded from both sides," says Ronald Atlas, head of the Center for Deterrence of Biowarfare and Bioterrorism at the University of Louisville in Kentucky. "Some say that this sort of research is dangerous because of the risk of the virus escaping or being using in bioterrorism, and others that it's good science."
Behold, happy is the man whom God correcteth: therefore despise not thou the chastening of the Almighty: For he maketh sore, and bindeth up: he woundeth, and his hands make whole ; He shall deliver thee in six troubles: yea, in seven there shall no evil touch thee. - Job 5

Offline TahoeBlue

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http://www.chinaeconomicreview.com/industry-focus/latest-news/article/2007-05-09/Pig_vaccinations_ordered_after_mystery_outbreak.html
POST ON 2007-05-09

Pig vaccinations ordered after mystery outbreak

Pig farmers were ordered to carry out mass vaccinations Tuesday following a mysterious outbreak in southern Guangdong province which killed up to 300 of the animals, AFP reported. The Agriculture Ministry said it had called for increased vaccinations for swine fever, pig rash and swine pneumonia as well as asking animal drug producers to boost their output. The pigs that succumbed to the disease in Guangdong first stopped eating and then developed fevers and began hemorrhaging, according to state media. The head of the local township where the outbreak took place said that there were up to 10,000 pigs in the township, but denied reports that up to 80% of the pigs had died. After news of the situation broke, local residents turned their backs on pork for fear of contamination.
Behold, happy is the man whom God correcteth: therefore despise not thou the chastening of the Almighty: For he maketh sore, and bindeth up: he woundeth, and his hands make whole ; He shall deliver thee in six troubles: yea, in seven there shall no evil touch thee. - Job 5

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http://www.politicalfriendster.com/showConnection.php?id1=7646&id2=2902

Connection between Swine Flu H1N1 and U. S. Department of Agriculture

May 1, 2004 “Modified‑live‑virus vaccines generated through reverse genetics can stimulate a better, broader immune response than killed‑virus vaccines.” There is a trade‑off, however, in that modified‑live‑virus vaccines may not be as safe as killed‑virus vaccines. “There’s always a chance a modified‑live‑virus vaccine may gain virulence as it replicates in the vaccinated host,” Richt says. 

http://www.porkmag.com/news_editorial.asp?pgID=675&ed_id=2800

Editor’s Note: The writer is a member of the Information Staff of the USDA Agricultural Research Service. This article has been edited from information in an article originally published in the February 2004 issue of Agricultural Research.

Reverse genetics may be a key for unlocking flu vaccine
By Luis Pons | Saturday, May 01, 2004

Scientists hope that the knowledge gained from using reverse genetics to explore individual components of the swine flu virus canultimately lead to new swine influenza vaccines.

USDA Agricultural Research Service (ARS) scientists studying a strain of swine influenza new to this part of the world have found that taking one step backward can lead to many steps forward.

Veterinary medical officers Jürgen Richt and Kelly Lager of the ARS National Animal Disease Center (NADC) in Ames, Iowa, are using a process called reverse genetics to gain insight into the rapid spread throughout North America of a swine flu type that contains gene segments from birds and humans as well as from pigs.

The researchers, who work in NADC’s Virus and Prion Diseases of Livestock Research Unit, are using reverse genetics to create new flu viruses in efforts to explore individual components of the virus. The hope is that vaccines can in turn exploit these components.

Jürgen Richt (left) and veterinary medical officer Kelly Lager use a laryngoscope to ianoculate an anesthetized pig, while Deborah Clouser observes.

Reverse genetics has been developed over the past decade for virus studies. “The technology has now advanced to where one can confidently generate influenza viruses entirely from cloned DNA resulting from the process,” says Lager. Richt adds that this work is unique because, while the process has been used on human flu strains, it has never been used on swine flu.

Genetic challenge
Swine influenza presents a special challenge in genetics because its genome comprises eight segments of ribonucleic acid, better known as RNA. RNA viruses such as swine flu store their genetic information in RNA, which is more susceptible to mutation than DNA. This allows RNA viruses to evolve far more rapidly than DNA viruses and sometimes makes it hard for an infected host to develop lasting immunity.

What made reverse genetics attractive for exploring the new swine flu strains is that manipulations commonly done on DNA cannot be performed with RNA.

That’s where the “reverse” in reverse genetics comes in. “Scientists can convert RNA viruses’ genetic material into a DNA state,” says Richt. “This is called reverse transcription. At this point, mutations can be introduced into the resulting cloned DNA. Once the DNA is converted back into RNA, the introduced mutations will occur in the genome of the RNA virus. Through this approach, we use cloned DNA to generate swine influenza viruses,” says Richt.

Iowa State University veterinary pathologist Bruce Janke, a swine influenza expert, is collaborating with USDA scientists in SIV research.

Richt and Lager – collaborating with veterinary pathologist Bruce H. Janke, Iowa State University and virologist Richard J. Webby, St. Jude Children’s Research Hospital in Memphis, Tenn. – generated the A/Swine/Texas/4199‑2/98 virus, or TX/98 for short.
“When tested in experimentally infected pigs, this generated virus showed characteristics similar to its parental wild type,” Richt says. In addition, pigs infected with TX/98 viruses that were genetically altered through mutation or deletion showed significantly less evidence of flu infection, according to Lager. “This makes these viruses potential candidates for modified‑live vaccines,” Lager adds.

Swine influenza is among the type A influenza viruses that can affect humans as well as chickens, ducks, horses, seals, whales and other animals.

Veterinary medical officer Jürgen Richt removes embryonated chicken eggs from an incubator. These eggs are used to propagate swine influenza A viruses.

New strain
As you are aware, specialists in North America used to diagnose almost exclusively only one type of flu virus in pigs: H1N1. That changed in 1998, when pigs started to be diagnosed with H3N2, a strain that up to that time was rarely seen here.

Since then, Lager says, these H3N2 viruses have combined, or reassorted, further with the classical H1N1 viruses, resulting in new H1N2 and H1N1 swine influenza viruses. The increased virulence represented by this new strain also has been a concern, he adds.

The H3N2 virus appeared in two types: a double reassortant (DR), labeled as such because it contains gene segments from both human and swine flu; and a triple reassortant (TR) that also contains gene segments from avian viruses. Richt says it’s the TR viruses that are causing most of the trouble. “By the end of 1999, these had spread throughout the United States, whereas the DR viruses had not,” he says.

Technician Deborah Clouser prepares purified plasmids containing individual swine influenza A virus gene segments for constructing a live swine influenza A virus.

Role of birds
Birds play an important role in the flu dynamic, providing a global reservoir of A‑type viruses. It is believed flu resides harmlessly in (most) birds, where viruses are genetically stable. When a virus from birds infects pigs that are already infected with a swine influenza virus, gene segments from each virus can be mixed, and a new influenza virus can arise. This reassortment likely produced the TR H3N2 virus.

Richt and Lager believe reverse genetics can greatly benefit the study of influenza in humans as well as in pigs.

“Current human and swine vaccines are inactivated vaccines that vary in efficacy, depending on the match of the vaccine with influenza virus strains circulating in the susceptible population,” says Richt. “Modified‑live‑virus vaccines generated through reverse genetics can stimulate a better, broader immune response than killed‑virus vaccines.”

In studies to construct a swine flu vaccine, cells are observed for signs of change that indicate a live swine influenza A virus was generated by reverse genetics.

There is a trade‑off, however, in that modified‑live‑virus vaccines may not be as safe as killed‑virus vaccines. “There’s always a chance a modified‑live‑virus vaccine may gain virulence as it replicates in the vaccinated host,” Richt says.

“But if a modified‑live‑influenza‑virus vaccine can be developed, it may be an important tool in preventing flu in pigs and humans. We also believe reverse genetics can contribute to our understanding of how influenza virus causes disease in various host species.”
Behold, happy is the man whom God correcteth: therefore despise not thou the chastening of the Almighty: For he maketh sore, and bindeth up: he woundeth, and his hands make whole ; He shall deliver thee in six troubles: yea, in seven there shall no evil touch thee. - Job 5

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http://www.unipr.it/arpa/facvet/dip/dipsa/ric/prrs2003/260-261.pdf
4th International Symposium on Emerging and Re-emerging Pig Diseases – Rome June 29th – July 2nd, 2003

SEROLOGICAL AND VIROLOGIC SURVEILLANCE FOR SWINE INFLUENZA VIRUS INFECTIONS AMONG PIGS OVER LARGE AREAS IN CHINA IN 1998~2002

Introduction
Influenza viruses have been isolated from a number of different animal hosts including birds, humans, horses, whales, minks, and pigs. Pigs have been postulated to play an important role in the process of genetic reassortment by acting as the "mixing vessel"[1].

Influenza in swine was first observed in the United States during the catastrophic 1918 human influenza pandemic, it is a commonly acute respiratory disease whose severity depends on many factors including pig age, virus strain, and secondary infections.

The classic SIV strain, H1N1, is local pandemic in Europe and America continental and spread to Taiwan, Hong Kong, and the continental in China and Japan in 1970s.

In 1979, the like-avian H1N1 SIV began to spread in swine in Europe and later spread to Asia, including China.

The SIV H3N2 subtype was first reported in Taiwan in 1969. The SIV H3N2 strains were isolated from pig flocks in northeast areas in China[2].

Pigs are susceptible to experimental infection with all subtypes of avian influenza A viruses and H9N2 influenza viruses have been isolated from pigs in Hong Kong.

H1N1 and H3N2 swine influenza viruses have been isolated from children in Holland and Hong Kong SAR of China[3].

Recently, the avian influenza has become very serious and complicated in many countries. A number of influenza viruses, including H1, H3, H5, H9 and H14, have been isolated from avian in China[4].

Influenza H3N2 virus, isolated from a young child in Hong Kong, was shown to be closely related to viruses circulating in European pigs[4].

Pigs are permissive to both human and avian influenza viruses and have been proposed to be an intermediate host for the genesis of pandemic influenza viruses through reassortment or adaptation of avian viruses[5].

Influenza virus infection in pigs is both an animal health problem and a public health concern. To gain insight into the molecular epidemiology, genetic evolution of SIV and spread of SI in China, serological and etiological studies of SI were carried out in 19 provinces and cities including Heilongjian, Jilin, Liaoning, Shandong, Inner Mongolia, Jiangsu, Anhui, Henan, Hebei, Zhejiang, Fujiang, Hainan, Hubei, Hunan, Guangdong, Guangxi, Zhongqing, Shanghai and Beijing.

Results indicated pig flocks in China were extensively infected with H3 subtype SI. H1, H3 and other subtypes of SIV co-existed in population in Provinces of Helongjiang, Fujian, Zhejiang, Guangdong, Inner Mongolia, et al.
Behold, happy is the man whom God correcteth: therefore despise not thou the chastening of the Almighty: For he maketh sore, and bindeth up: he woundeth, and his hands make whole ; He shall deliver thee in six troubles: yea, in seven there shall no evil touch thee. - Job 5

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Ok, they released a California sequence, but has any sequence from Mexico been published? i.e. How do we know they are the same?

http://www.freerepublic.com/focus/news/2237650/posts

http://www.who.int/csr/disease/swineflu/en/

Viral gene sequences to assist update diagnostics for swine influenza A(H1N1)
http://www.who.int/entity/csr/resources/publications/swineflu/sequences/en/index.html
28 April 2009
http://www.who.int/csr/disease/swineflu/swineflu_genesequences_20090425.pdf

Viral gene sequences to assist update diagnostics for swine influenza A(H1N1)
25 April 2009
WHO published a Guidance to influenza laboratories on response to swine influenza
A(H1N1) infections1. Due to the fact that it is a new reassortant virus, diagnostics has to be updated accordingly.

The full genome sequence of the newly identified swine influenza virus A/California/04/2009 A(H1N1) has been made available by the WHO Collaborating Center in CDC, Atlanta, USA on the GISAID sequence database2 and has the following accession numbers.

Further update on availability on other public sequence databases will be provided when available.
Behold, happy is the man whom God correcteth: therefore despise not thou the chastening of the Almighty: For he maketh sore, and bindeth up: he woundeth, and his hands make whole ; He shall deliver thee in six troubles: yea, in seven there shall no evil touch thee. - Job 5

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http://www.virology.ws/2009/04/29/swine-influenza-daily-update/

Swine influenza daily update
by vrr on 29 April 2009

Here is an update on the global swine flu situation as of 28 April 2009.

There are now 64 laboratory confirmed cases of infection with the H1N1 swine influenza strain, up from 40 the day before. States reporting cases are California (10), Kansas, (2), New York City (45), Ohio (1) and Texas (6). These are the same states that reported isolations on the previous day. There are new laboratory confirmed isolations of the virus in Australia (3), Israel (1, a traveler returning from Mexico), and New Zealand (3). The number of laboratory confirmed cases in Mexico remains the same as the previous day: 26 cases, 7 deaths. This brings the total number of countries reporting laboratory confirmed cases to seven.

Swine influenza virus isolates from the US and Mexico have been given names according to the proper nomenclature, which takes the following form:
Influenza type/Country/isolate number/year (subtype).

Accordingly, the following swine influenza virus strains have been isolated:

A/California/04/2009 (H1N1)
A/California/06/2009 (H1N1)
A/California/07/2009 (H1N1)
A/California/08/2009 (H1N1)
A/California/10/2009 (H1N1)
A/Texas/04/2009 (H1N1)
A/Texas/05/2009 (H1N1)
A/Kansas/03/2009 (H1N1)
A/Ohio/07/2009 (H1N1)
A/New York/19/2009 (H1N1)
A/New York/20/2009 (H1N1)
A/Mexico/4482/2009 (H1N1)
A/Mexico/4486/2009 (H1N1)
A/Mexico/4108/2009 (H1N1)
A/Mexico/4115/2009 (H1N1)
A/Mexico/4603/2009 (H1N1)
A/Mexico/4604/2009 (H1N1)

I expect to see many more isolates from different countries in the coming weeks.

Today the CDC released genome sequences of the viral RNAs of six swine flu isolates from California and Texas (Addendum: sequences of New York, Ohio, and Kansas isolates were added late yesterday). The influenza virus genome consists of eight segments of RNA, each coding for one or more proteins (illustrated). Each RNA segment has a name - PB2, PB1, PA, HA, NP, NA, MP, and NS. Mystery Rays has done a quick analysis of the sequences. The isolates are all the same strain, but they are not identical.

 Unfortunately we don’t yet have genome sequence from any Mexican isolate - otherwise we could determine if they are significantly different.

Such information might provide clues about why the disease in Mexico seems to be more severe than elsewhere.

A comparison with RNA sequences of other influenza virus isolates shows that most of the viral RNAs are from swine influenza viruses, with the possible exception of the PB1 RNA, which may be derived from a human H1N1 virus.

 This observation is somewhat surprising, because last week we were told that the new swine virus had RNA segments from pig, human, and avian influenza viruses.

According to ProMED-mail, the NA and MP genes are related to those of influenza viruses from Asian-European swine, and the other genes appear to originate from swine flu viruses from pigs in North America.

The data are in accord with the original assertion of the CDC that all genes of the new isolate were derived from swine viruses.

The fact that A/California/04/2009 and related isolates are pig viruses, with little or no genetic material from human influenza virus strains, is fascinating.

Clearly these strains are different from viruses that circulate in pigs because they can be transmitted among humans and cause respiratory disease. It will be very important to compare the sequences of these isolates with viruses obtained from pigs in an attempt to determine what changes enabled the virus to adapt to humans.

Comments:

 
Quote
Is it true there are zero avian flu components in these US isolates?

Yes, according to the sequences that have been submitted so far.
Behold, happy is the man whom God correcteth: therefore despise not thou the chastening of the Almighty: For he maketh sore, and bindeth up: he woundeth, and his hands make whole ; He shall deliver thee in six troubles: yea, in seven there shall no evil touch thee. - Job 5

Offline TahoeBlue

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http://www.virology.ws/2009/04/30/swine-flu-amexico2009-h1n1-questions-and-answers/
Swine flu A/Mexico/2009 (H1N1): Questions and answers
by vrr on 30 April 2009
...

Q: I found these statistics on the newspaper “Reforma” so I have added the population for each state (in thousands) and calculated morbidity and mortality by adding all up (deaths, proven cases and probable (maybe) cases) and it turns out that the states with the highest morbidity do not have the highest mortality… for instance Tlaxcala has the highest morbidity for such a small state and San Luis Potosi has the highest mortality with a much lower morbidity….

Q. Could be that we are dealing with two different types of H1N1 viruses? one is the California that is not too virulent and a mutated one that is highly virulent and is not spreading that much….

A: These are certainly possible scenarios. Until we have sequences from the Mexican isolates we won’t know the answers.  I do think the absence of sequence information from Mexico is exacerbating the panic.
Behold, happy is the man whom God correcteth: therefore despise not thou the chastening of the Almighty: For he maketh sore, and bindeth up: he woundeth, and his hands make whole ; He shall deliver thee in six troubles: yea, in seven there shall no evil touch thee. - Job 5

Offline TahoeBlue

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http://forum.prisonplanet.com/index.php?topic=101338.msg624127#msg624127

http://thedailybite.wordpress.com/2009/05/05/canadian-scientists-infect-pigs-with-deadly-zombie-virus-from-1918-spanish-h1n1-flu-pandemic/

Canadian scientists infect pigs with deadly Zombie virus from 1918 ‘Spanish’ H1N1 flu pandemic

May 5, 2009 ·
Hot off the Journal of Virology Press!!!

Experimental Infection of Pigs with the Human 1918 Pandemic Influenza Virus

“Swine influenza was first recognized as a disease entity during the 1918 “Spanish flu” pandemic. The aim of this work was to determine the virulence of a plasmid-derived human 1918 pandemic H1N1 influenza virus (reconstructed 1918, or 1918/rec, virus) in swine using a plasmid-derived A/swine/Iowa/15/1930 H1N1 virus (1930/rec virus), representing the first isolated influenza virus, as a reference. Four-week-old piglets were inoculated intratracheally with either the 1930/rec or the 1918/rec virus or intranasally with the 1918/rec virus. A transient increase in temperature and mild respiratory signs developed postinoculation in all virus-inoculated groups. In contrast to other mammalian hosts (mice, ferrets, and macaques) where infection with the 1918/rec virus was lethal, the pigs did not develop severe respiratory distress or become moribund.
….
Presented data support the hypothesis that the 1918 pandemic influenza virus was able to infect and replicate in swine, causing a respiratory disease, and that the virus was likely introduced into the pig population during the 1918 pandemic, resulting in the current lineage of the classical H1N1 swine influenza viruses.

Nostalgia has its place, but raising a lethal virus from the dead and infecting little piglets with it seems to take longing for the bad old days a bit far. Can’t blame Canada for the Zombie virus idea, though. The initial effort was led by a molecular pathologist at the Armed Forces Institute of Pathology in Rockville, Maryland. He and his team spent 10 years piecing together the deadly virus in a lab at the CDC in Atlanta.

They built their Zombie virus from pieces of wax-encased lung tissue that were preserved from the autopsies of two soldiers who were among the 1918 flu’s 675,000 American victims, and also from the frozen body of an Inuit woman buried in the Alaska permafrost after dying from the virus in November of 1918.

Oh, and we can’t blame the Spanish, either, for the 1918 ‘Spanish’ flu pandemic. The Irish Examiner reports about the real origin of that catastrophe here.

“Ryle would have us believe that all those American soldiers who died from non-combatant causes may have died from Spanish flu.

But US Army records show that seven men dropped dead after being vaccinated.

A report from US Secretary of War Henry L Stimson not only verified these deaths but also stated that there had been 63 deaths and 28,585 cases of hepatitis as a direct result of yellow fever vaccination during only six months of the war.

That was only one of the 14 to 25 shots given to recruits.

Army records also reveal that after vaccination became compulsory in the US Army in 1911, not only did typhoid increase rapidly but all other vaccinal diseases increased at an alarming rate.
…..
The army doctors knew all these cases of disease and death were due to vaccination and were honest enough to admit it in their medical reports.

When army doctors tried to suppress the symptoms of typhoid with a stronger vaccine, it caused a worse form of typhoid paratyphoid.   But when they concocted an even stronger vaccine to suppress that one, they created an even worse disease - Spanish flu.

After the war, this was one of the vaccines used to protect a panic-stricken world from the soldiers returning from WWI battlefronts infected with dangerous diseases.

Funny how a few short years after the Zombie virus was resurrected that a another mysterious new H1N1 virus has flashed around the globe. And some scientists have even said that this new virus is very similar to the Zombie virus.

According to the biodefense watchdog group, The Sunshine Project, the risk and suffering to experimental animals involved in recreating the 1918 virus are unjustified.  http://www.sunshine-project.org/

“(Austin and Hamburg, 9 October 2003) – The ‘Spanish Flu’ influenza virus that killed 20-40 million people in 1918 is currently under reconstruction. Several genes of the extraordinarily lethal 1918 flu virus have been isolated and introduced into contemporary flu strains. These proved to be lethal for mice, while virus constructs with genes from a current flu virus types had hardly any effect. These experiments may easily be abused for military purposes, but provide little benefit from a medical or public health point of view….”

Unfortunately you’ll note that the Sunshine Project is no longer shining its light on mistakes and accidental releases of deadly pathogens by biodefense research labs. Their work ended without explanation a few months after they reported a series of violations made by a lab in Texas. At least their website is archived for now.

Makes you wonder where this new ‘mutt’ H1N1 virus really originated, doesn’t it?

Well, main thing to remember is that if Canadian scientists are doing the cooking…

http://www.sunshine-project.org/
Quote
As of 1 February 2008, the Sunshine Project is suspending its operations.
Although this website is no longer updated, it remains online as an archive of our activities and publications from 2000 through 2008.
If you have any questions, please contact us by e-mail at [email protected]
Behold, happy is the man whom God correcteth: therefore despise not thou the chastening of the Almighty: For he maketh sore, and bindeth up: he woundeth, and his hands make whole ; He shall deliver thee in six troubles: yea, in seven there shall no evil touch thee. - Job 5

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http://www.cdc.gov/ncidod/eid/vol12no01/05-0979.htm

History

1918 Influenza: the Mother of All Pandemics
Jeffery K. Taubenberger* and David M. Morens 
*Armed Forces Institute of Pathology, Rockville, Maryland, USA; and  National Institutes of Health, Bethesda, Maryland, USA
...

http://jvi.asm.org/cgi/content/full/83/9/4287

Journal of Virology, May 2009, p. 4287-4296, Vol. 83, No. 9
0022-538X/09/$08.00+0     doi:10.1128/JVI.02399-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.


Experimental Infection of Pigs with the Human 1918 Pandemic Influenza Virus

Hana M. Weingartl,1,2* Randy A. Albrecht,3 Kelly M. Lager,4 Shawn Babiuk,1,5 Peter Marszal,1 James Neufeld,1 Carissa Embury-Hyatt,1 Porntippa Lekcharoensuk,4,10 Terrence M. Tumpey,6 Adolfo García-Sastre,3,7,8 and Jürgen A. Richt4,9*
National Centre for Foreign Animal Disease, Canadian Food Inspection Agency, Winnipeg, Manitoba, Canada,1 Department of Medical Microbiology,2 Department of Immunology, University of Manitoba, Winnipeg, Manitoba, Canada,5 Department of Microbiology,3 Department of Medicine, Division of Infectious Diseases,7 Emerging Pathogens Institute, Mount Sinai School of Medicine New York, New York,8 National Animal Disease Center, ARS-USDA, Ames, Iowa,4 Centers for Disease Control and Prevention, Influenza Division, Atlanta, Georgia,6 Kansas State University, College of Veterinary Medicine, Manhattan, Kansas,9 Department of Microbiology and Immunology, Faculty of Veterinary Medicine, Kasetsart University, Bangkok, Thailand,10

Received 19 November 2008/ Accepted 6 February 2009

ABSTRACT

Swine influenza was first recognized as a disease entity during the 1918 "Spanish flu" pandemic. The aim of this work was to determine the virulence of a plasmid-derived human 1918 pandemic H1N1 influenza virus (reconstructed 1918, or 1918/rec, virus) in swine using a plasmid-derived A/swine/Iowa/15/1930 H1N1 virus (1930/rec virus), representing the first isolated influenza virus, as a reference. Four-week-old piglets were inoculated intratracheally with either the 1930/rec or the 1918/rec virus or intranasally with the 1918/rec virus. A transient increase in temperature and mild respiratory signs developed postinoculation in all virus-inoculated groups. In contrast to other mammalian hosts (mice, ferrets, and macaques) where infection with the 1918/rec virus was lethal, the pigs did not develop severe respiratory distress or become moribund. Virus titers in the lower respiratory tract as well as macro- and microscopic lesions at 3 and 5 days postinfection (dpi) were comparable between the 1930/rec and 1918/rec virus-inoculated animals. In contrast to the 1930/rec virus-infected animals, at 7 dpi prominent lung lesions were present in only the 1918/rec virus-infected animals, and all the piglets developed antibodies at 7 dpi. Presented data support the hypothesis that the 1918 pandemic influenza virus was able to infect and replicate in swine, causing a respiratory disease, and that the virus was likely introduced into the pig population during the 1918 pandemic, resulting in the current lineage of the classical H1N1 swine influenza viruses.

 INTRODUCTION


As the 1918 "Spanish flu" pandemic spread through the central United States, a swine respiratory disease was concurrently observed in this region. The swine disease was highly contagious; it had high morbidity with fever, anorexia, dyspnea, cough, and prostration, with sudden onset and fast recovery within 2 to 6 days after first clinical signs, and low mortality (between 1 and 4%). Due to a strong resemblance of the clinical signs to the human influenza disease, a clinical name of "hog flu" was given by J. S. Koen to this new disease of pigs (15, 27). Similar swine respiratory diseases suspected to be influenza were reported at about the same time in Europe and China (2).

Following the human pandemic, hog flu or, in today's terminology, swine influenza was reported intermittently in the Midwest of the United States. In 1930 swine H1N1 influenza virus (A/swine/Iowa/14 and A/swine/Iowa/15/1930) was isolated from diseased pigs and was demonstrated to play a critical role in the disease although severity often depended on secondary bacterial infections (27, 28).

Early serological studies linked the first human H1N1 influenza virus isolates (e.g., PR8/1934) and, even more so, the swine H1N1 1930 virus isolate to the 1918 pandemic virus (5, 30). Laidlaw (15) suggested that the swine influenza virus could be the 1918 pandemic influenza virus which became established in pigs. Recent phylogenetic analyses of the 1930 swine flu virus, the first human H1N1 influenza virus isolates, the classical H1N1 swine influenza viruses, and the reconstructed 1918 human influenza virus (1918/rec virus) (37) strongly support the originally proposed hypothesis as all these viruses appear to be derived from a common source, the 1918 pandemic virus (7, 34, 41). Interestingly, the 1930 swine influenza virus may still be circulating in swine (1). Although the origin of the 1918 virus is not known, it has been suggested that the virus came from an avian reservoir and either entered the human population directly or indirectly through an intermediate host (34).

Swine have been proposed as an intermediate host in the indirect transmission of influenza A viruses from an avian reservoir to humans, based on the unique distribution in pigs of 2,3- and 2,6-linked sialic acid moieties that are considered to be avian- and human-specific receptors for influenza A viruses, respectively. The presence of the avian and human receptors in the swine respiratory tract can enable the pigs to become infected with either avian or human influenza A viruses, setting the stage for reassortant events between swine, avian, and human viruses or for adaptation of an avian virus to a mammalian receptor (20). Support for this hypothesis can be found in the isolation of entirely avian or human viruses from swine, as well as reassortant viruses that contain swine, human, and avian genes (2, 13, 22, 42, 43). Reports also document interspecies transmission from pigs to people (21, 42). However, even though the 1957 and 1968 human pandemic viruses were human-avian reassortants, there is no evidence that the reassortment occurred in pigs. This classical theory was based on contemporary knowledge of receptor distribution in different host species, and it has been recently questioned, particularly in light of the proven direct transmission of avian influenza virus to humans (40).

Recently, the 1918/rec virus (14, 37) was demonstrated to be highly pathogenic in mice (37), ferrets (38), and nonhuman primates (14). This report describes experimental infection of swine with the 1918 influenza virus with the hemagglutinin of the 1918 South Carolina influenza virus isolate in comparison to the H1N1 swine influenza virus isolate from the year 1930. The A/swine/Iowa/15/1930 was chosen as a reference virus because it is thought to be a descendant of the 1918 pandemic influenza virus. The aim of this work was to gain some insight into influenza infections of swine during the 1918 influenza pandemic by determining whether the 1918 human influenza virus can infect and replicate in swine and cause clinical disease and lesions in the infected animals.


MATERIALS AND METHODS


All live virus work with the 1918/rec pandemic influenza virus was performed in the biosafety level 4 laboratory and animal cubicle at the National Centre for Foreign Animal Disease (NCFAD).

Viruses. Viruses used in this study were rescued using reverse genetics. Plasmids for the influenza viruses were transfected into cocultures of MDCK and 293T cells using Lipofectamine 2000 (Invitrogen) as described by Schickli et al. (25). The generation of infectious influenza virus from the transfections was assessed by plaque assay of the culture supernatants on MDCK cells.

(i) H1N1 1918/rec virus. Although the H1N1 1918/rec virus was previously rescued at the CDC (37), in order to perform the studies at NCFAD, the virus was rerescued using the same pPol-I rescue plasmids directing the synthesis of negative-sense (virion RNA) genomic-length transcripts of the eight genomic segments of the 1918 influenza virus and supporting pCAGGS expression plasmids encoding the A/WSN/33 polymerase subunits (PB1, PB2, and PA) and nucleocapsid protein NP. The rescue plasmid used for hemagglutinin (HA) encoded the HA gene of the 1918 South Carolina influenza virus isolate with a receptor binding specificity for 2,6-linked sialic acids (6, 37). Reverse transcription-PCR (RT-PCR) and sequencing confirmed that the genome of the rescued virus was identical in sequence to the cDNA in the plasmids used for its rescue.

(ii) H1N1 1930/rec virus (A/swine/Iowa/15/1930). The plasmid pHW2000/pDZ (9) that directs the synthesis of negative-sense (virion RNA) and positive-sense (cRNA) genomic-length influenza virus transcripts was utilized to create a set of eight rescue plasmids for the A/swine/Iowa/15/1930 (H1N1) influenza virus (17). Novel restriction enzyme sites were introduced into each gene segment in order to differentiate the rescued 1930/rec virus from the wild-type virus.

Virus titers were determined by endpoint titration on monolayers of MDCK cells in 96-well microtiter plates (Costar; Corning). Briefly, 50 µl of 10-fold serial dilutions of virus samples in alpha-minimal essential medium-0.3% bovine serum albumin supplemented with 10 U/ml of TPCK (tosylsulfonyl phenylalanyl chloromethyl ketone)-treated trypsin (Sigma) was incubated on the cells for 1 h at 30°C in 5% CO2. Following the virus adsorption, an additional 50 µl of alpha-minimal essential medium-0.3% bovine serum albumin supplemented with 10 U/ml of TPCK-trypsin was added to each well, and the plates were incubated as described above for 5 days. The 50% tissue culture infective dose (TCID50) was determined using the method of Reed and Muench.

Animal inoculations. (i) Mice. Female BALB/c mice, 6 to 7 weeks old (Charles River Laboratories, Wilmington, MA), were anesthetized with an intraperitoneal injection of 0.2 ml of 2,2,2-tribromoethanal in tert-amyl alcohol (Avertin; Aldrich Chemical Co., Milwaukee, WI.). Ten mice per each treatment group were inoculated intranasally with 50 µl/104 TCID50/animal of either 1918/rec or 1930/rec virus, or mock inoculated with phosphate-buffered saline (PBS). Individual body weights and clinical signs were recorded each day postinfection (dpi) up to 8 dpi. At the end of the experiment, surviving mice were euthanized by intraperitoneal injection of an overdose of ketamine hydrochloride (200 mg/kg). Whole lungs were collected for virus RNA detection.

(ii) Swine. The pregnant sows and then the piglets were tested on the farm for antibodies against H3N2 and H1N1 by Idexx enzyme-linked immunosorbent assay to confirm the swine influenza virus-free status of the high-health status herd at Designed Genetics, Lockport, Manitoba (Canada). The 3-week-old piglets were retested upon arrival at the NCFAD for influenza virus-specific antibodies using the HerdCheck Swine Influenza Virus (H1N1) Antibody Test Kit (Idexx Laboratories) according to the manufacturer's instructions. The animals were acclimatized for 7 days and inoculated either intratracheally (1 ml) or intranasally (2 ml) with 105.4 TCID50 of 1918/rec or 1930/rec influenza virus/animal or mock inoculated with PBS. Six piglets were inoculated intratracheally, and 12 were inoculated intranasally with the 1918/rec virus (a total of 18 piglets). Twelve piglets were inoculated intratracheally with the same dose of the 1930/rec virus, and 12 control piglets were mock inoculated with PBS. Body temperatures and clinical signs were recorded daily. Piglets inoculated with the 1918/rec virus were sampled and euthanized at 3, 5, and 7 dpi or at 3, 5, 7, 12, and 17 dpi; 1930/rec virus- and PBS-inoculated pigs were euthanized and sampled at 3, 5, and 7 dpi. Blood/serum, oropharyngeal swabs, nasal swabs or washes, bronchoalveolar lavage fluid (BALF), and the following tissues were collected: heart, brain, digestive tract samples, kidney, urine, liver, muscles, tonsil, thymus, spleen, cerebrospinal fluid, feces, submandibular and bronchial lymph nodes, trachea, and lung. The experimental design is summarized in Table 1.

All animal manipulations were approved by the Animal Care Committee of the Canadian Science Centre for Human and Animal Health, according to the guidelines of the Canadian Council on Animal Care.
Gross pathology. Pathological changes were evaluated in all major organs of all piglets at the time of necropsy. Photographic images of lungs were taken from most of the piglets. The extent of the macroscopic lesions on the lung surfaces was visually evaluated based on the photographic images or directly during the necropsy and is expressed as a percentage of the entire lung using the Ambico, Inc. Lung Score Sheet.

Histopathology and immunohistochemistry (IHC). Tissue samples were fixed in 10% neutral phosphate-buffered formalin, routinely processed, and stained with hematoxylin and eosin (H&E) following standard protocols.

Formalin-fixed paraffin-embedded tissue sections were pretreated with proteolytic enzyme (DakoCytomation) for 15 min prior to immunostaining. Monoclonal antibody specific for the nucleoprotein of influenza A virus (ME Clone 1331; Biodesign Sasco) was used at a dilution of 1:5,000 to detect the viral antigen and visualized using the Envision anti-mouse (horseradish peroxidase labeled) polymer kit (DakoCytomation) reacted with the chromogen diaminobenzidine. Tissues were counterstained with Gill's hematoxylin. IHC slides were scored from 0 to 4+ as follows: 1+, occasional positive bronchiolar epithelial cells; 2+, <25% of bronchioles having positive cells; 3+ 25 to 75% of bronchioles having positive cells; 4+, >75% of bronchioles having positive cells.

Virus isolation. Virus isolation on MDCK cells was attempted from BALF and from clarified 10% (wt/vol) lung homogenates in PBS as described above in the paragraph on virus titer determinations.

Nine-day-old embryonated eggs were inoculated via the allantoic cavity with 0.2 ml of undiluted clarified BALF and incubated until embryo death or up to 5 dpi.

Real-time RT-PCR. Probe and primers targeting the matrix protein were used in the real-time RT-PCR detection of viral RNA (23, 31) on all samples listed in the paragraph on swine inoculations above. Viral RNA was extracted from samples according to the manufacturer's instructions using TriPure Isolation Reagent (Roche Applied Science, Indianapolis, IN).

Hemagglutination inhibition was used to characterize the rescued viruses and to determine serum antibodies in the infected piglets. The microtiter HA and hemagglutination inhibition (HI) assays were performed by standard protocols using a 0.5% suspension of chicken red blood cells in PBS. Sera serially diluted twofold were tested against 4 HA units of the respective H1N1 virus. Serum against influenza A/mallard/ON/629/2005 (H1N1) virus that cross-reacted with the influenza 1930/rec virus to a titer of 80 to 160 was used as a positive control.

The HA identities of the rescued 1918/rec and the 1930/rec viruses were verified with mouse monoclonal antibodies using the same assay format as above. The monoclonal antibody 5D3 recognized both 1918 and 1930 HA, and 58F4E10 recognized 1918 HA (unpublished data).


 RESULTS

Infection of mice. The virulence of the rescued viruses was initially confirmed in mice before inoculation of swine. Mice were inoculated intranasally with 104 TCID50/animal with either the 1918/rec or 1930/rec virus or mock inoculated with PBS. All mice inoculated with the 1918/rec virus died by 8 dpi, as expected based on the previous characterization of the 1918/rec virus (37). The 1930/rec virus was also highly virulent for mice. Seven out of 10 inoculated mice died by 6 dpi; the remaining animals survived until the end of the experiment (8 dpi) (Fig. 1). The three surviving mice continued losing weight, their respiratory rate remained elevated, and their fur was ruffled. Activity and water and food intake were decreased. The control PBS-inoculated mice did not exhibit clinical signs.

The lungs from the 1918/rec and the 1930/rec virus-infected mice collected at necropsy were severely hemorrhagic in appearance and friable while lungs from the control mice were normal. Virus replication in lungs of the infected mice was confirmed by real-time RT-PCR targeting the matrix gene. There was no significant difference in copy numbers between the 1918/rec and the 1930/rec virus-infected groups. Comparable threshold cycle numbers (approximately 23 to 24) indicated the presence of approximately 200,000 to 250,000 copies/g of the lung tissue (data not shown).
Infection of swine. There were no significant differences found between the animals inoculated intratracheally or intranasally with the 1918/rec virus, and for the purposes of this report, the two groups are discussed as one.

(i) Clinical signs. Clinical signs and rectal temperatures were recorded daily for all animals. Transient increase in body temperature and mild respiratory signs developed starting at 1 dpi in both influenza virus-inoculated groups but not in the control animals. Body temperatures above 39.9°C were considered above normal.

In both groups (1918/rec and 1930/rec virus infections), body temperatures above normal were observed postinoculation at 1 dpi and in some animals also between 4 to 6 dpi. Respiratory signs were observed in only the first group of piglets inoculated with the 1930/rec virus (animals no. 66 to 72) at 2 and at 5 dpi. Two pigs displayed abdominal breathing, and one of them was also sneezing at 2 dpi. None of the 1918/rec virus-inoculated animals, control animals, or the second group of the 1930/rec virus-inoculated animals displayed apparent clinical signs.

(ii) Gross pathology. Gross lung lesions, accompanied by enlarged tracheobronchial lymph nodes, were observed in both influenza virus-infected groups. The extent of the macroscopic lesions was comparable between the 1930/rec and 1918/rec virus-inoculated animals at 3 dpi. Starting at 5 dpi, the lung lesions were more severe in the 1918/rec virus-inoculated piglets than in the 1930/rec virus-inoculated animals, and appeared to be progressively more widespread at later time points (Fig. 2). Initially, the lesions were mostly located in the apical lobes, with some involvement of the cardiac lobes. In general, the lesions can be described as irregularly distributed, plum-colored consolidated depressions, corresponding to individual lobules. At 7 dpi lobular septae of the 1918/rec virus-inoculated piglets were prominent, suggesting mild edema. Some piglets had reticulated, gray-white bulging foci in several lobules, suggesting areas of inflammation centered on bronchioles. (Fig. 3) At later time points, the lung lesions in piglets inoculated with the 1918/rec virus spread also to the diaphragmatic lobes; at 12 and 17 dpi petechia and extensive multiple small spider-like hemorrhages were noted on the surfaces of the lungs, and blood was observed in the larger lung airways (trachea and bronchi). At 17 dpi the lungs had uniform purple discoloration of the diaphragmatic lobes, suggesting hypostatic congestion.

...


 DISCUSSION

The experimental work presented in this report demonstrated that the human 1918 influenza virus can infect and replicate in pigs and cause clinical disease and lesions in the infected animals. Combined with the original swine influenza outbreak descriptions, the early serological work, and the recent phylogenetic analyses, these results support the hypothesis that the 1918 human influenza virus and the virus causing the hog flu during the 1918 pandemic were the same.
The virulence of both the 1918 and the 1930 rescued recombinant viruses was first tested in mice to ensure that these viruses were phenotypically identical with the virus previously reconstructed at CDC, in the case of the 1918/rec virus (37), or with the original isolate as described by Shope, in the case of the 1930/rec virus (29). The high lethality observed in the inoculated mice confirmed the anticipated phenotypes of the viruses.

Interestingly, the 1918/rec virus, which is known to induce lethal infection upon experimental inoculation in ferrets and macaques (14, 38), was not highly virulent in pigs, indicating a potential resistance of swine to highly virulent influenza viruses. Experimental infections of pigs with highly pathogenic H5N1 avian viruses are also consistent with this notion (3, 19). Host factors appear to be critical in the resistance to virulent influenza viruses: BALB/c mice that carry a deletion in the Mx gene (Mx protein is a mediator of cellular resistance to influenza virus) (33) were highly susceptible to the infection with the reconstructed 1918 influenza virus (37), while mice carrying a wild-type Mx1 gene were able to restrict the virus replication (39).The functional Mx protein is expressed in the lungs of pigs experimentally infected with swine influenza virus (11), but our work does not exclude the possibility that additional host factors may have contributed to the high resistance against the 1918 pandemic influenza in pigs.

The early pathological changes and virus titers in both the 1918/rec and 1930/rec virus-infected pigs were considered consistent with typical swine influenza virus infections. No differences were observed between animals inoculated intratracheally (somewhat simulating aerosol inoculation by delivery of the virus into the lower respiratory tract) or intranasally with the 1918/rec virus; for example, the virus titers recovered from BALFs were within the same range for both inoculation routes. Interestingly, human volunteers experimentally inoculated by aerosol developed disease resembling natural influenza virus infections while the ones inoculated via nasal drops did not (36).

The relatively rapid antibody response (HI titers of 128 at 7 dpi) in the 1918/rec virus-infected animals, however, was a somewhat surprising finding as this is not usually reported for swine influenza virus. The more widespread and atypical lesions observed in lung of the 1918/rec virus-infected animals at later times postinfection, such as perivascular hemorrhages along with presence of blood in the airways and the gross lesions in the diaphragmatic lobes, were not expected and may be related to differences in immune response to the 1918/rec versus the 1930/rec virus. However, no conclusions were drawn based on these observations since only three animals were kept past 7 dpi, and we were not able to determine the factors involved in the pathological changes beyond 7 dpi in the 1918/rec virus-infected pigs. Interestingly, the original reports commented on the presence of pulmonary lesions in pigs slaughtered three weeks or more after clinical recovery from the hog flu (27).

Overall, the clinical disease and virus replication observed in piglets infected with the 1918/rec influenza virus were consistent with a typical swine influenza virus infection (12, 22, 23) and not significantly different from the infection with the 1930/rec virus, representing classical swine H1N1 viruses. The clinical signs observed in our 1930/rec virus-infected pigs corresponded with the description of the disease given by Shope for pigs inoculated with the 1930 filtered samples of swine influenza virus (27, 28). In his experimental inoculations, the respiratory disease was mild compared to the field infections in swine. Shope concluded that coinfection with Haemophilus influenzae suis was necessary to induce severe disease in swine (18, 27, 28). It is generally accepted that the clinical outcome of experimental and field infections with influenza virus in swine can differ as additional factors (e.g., stress or crowding) and agents (e.g., mycoplasma, respiratory bacteria, or other viruses) are usually involved in the field, worsening the disease signs caused by the virus. Based on historical records, the swine influenza in 1918 was not a severe disease although, due to almost 100% morbidity, the concerns about classical swine fever (where mortality at that time was reaching 75% in the affected herds) brought it strongly into focus (reference 4 and references therein; see also references 27 and 30). Thus, our observation of a mild clinical disease in piglets infected experimentally with the 1918/rec virus strengthens the hypothesis that the influenza in pigs during the pandemic was caused by the same (or very close) virus as the human influenza (5, 7, 15, 30, 35, 41).

The question of the role of swine in the 1918 influenza pandemic is very interesting. Our experimental infections demonstrated that the 1918 human influenza virus causes an apparent disease in swine, suggesting that this virus was not present unnoticed in pigs prior to the reported outbreaks. The historical records indicate that the disease in swine was observed only later during the pandemic (4), with the first notable occurrence in October 1918 (30). Consequently, one could speculate that the initial interspecies transmission of influenza virus during the 1918 pandemic occurred from people to pigs and only later appeared to occasionally transmit back to people (reference 4 and references therein), likely contributing at least regionally to the maintenance and spread of the disease. The virus spread throughout the swine population, adapted to the swine host, and subsequently resulted in the current lineage of the classical H1N1 swine influenza viruses (7, 26).

In summary, our study demonstrates that swine are susceptible to infection with the 1918 pandemic influenza virus; however, this species does not appear to be as sensitive to the virus as mice, ferrets, and nonhuman primates. It supports the hypothesis based on genetic analysis that the 1918 pandemic influenza virus is likely an ancestor of both the human H1N1 viruses and the classical swine H1N1 influenza viruses, both still present in humans and pigs.

Although the acute 1918 influenza virus infection was similar to the 1930 influenza virus infection and to other influenza virus infections reported in swine, there was an interesting difference in the convalescent phase. In this study lesions were detected as late as 20 dpi, suggesting that the 1918 virus may have unique virulence determinants in comparison to other swine influenza viruses.

ACKNOWLEDGMENTS

Funding for this work was provided from the Canadian Food Inspection Agency and ARS-USDA technical development funds.

We thank John Copps, Jason Gren, and Greg Smith for technical support.


FOOTNOTES


* Corresponding author. Mailing address for Hana M. Weingartl: National Center for Foreign Animal Disease, Canadian Food Inspection Agency, 1015 Arlington St., Winnipeg, Manitoba R3E 3M4, Canada. Phone: (204) 789 2027. Fax: (204) 789-2038. E-mail: [email protected]. Mailing address for Jürgen A. Richt: College of Veterinary Medicine, K224B Mossier Hall, Kansas State University, Manhattan, KS 66506. Phone: (785) 532-2793. Fax: (785) 532-4039. E-mail: [email protected]

Published ahead of print on 18 February 2009

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Swine Flu May Be Human Error; WHO Probes Scientist’s Claim

By Jason Gale and Simeon Bennett

May 13 (Bloomberg) -- The World Health Organization is investigating a claim by an Australian researcher that the swine flu virus circling the globe may have been created as a result of human error.

Adrian Gibbs, 75, who collaborated on research that led to the development of Roche Holding AG’s Tamiflu drug, said in an interview that he intends to publish a report suggesting the new strain may have accidentally evolved in eggs scientists use to grow viruses and drugmakers use to make vaccines. Gibbs said he came to his conclusion as part of an effort to trace the virus’s origins by analyzing its genetic blueprint.

The World Health Organization received the study last weekend and is reviewing it, Keiji Fukuda, the agency’s assistant director-general of health security and environment, said in an interview May 11. Gibbs, who has studied germ evolution for four decades, is one of the first scientists to analyze the genetic makeup of the virus that was identified three weeks ago in Mexico and threatens to touch off the first flu pandemic since 1968.

A virus that resulted from lab experimentation or vaccine production may indicate a greater need for security, Fukuda said. By pinpointing the source of the virus, scientists also may better understand the microbe’s potential for spreading and causing illness, Gibbs said.

Possible Mistake

“The sooner we get to grips with where it’s come from, the safer things might become,” Gibbs said by phone from Canberra yesterday. “It could be a mistake” that occurred at a vaccine production facility or the virus could have jumped from a pig to another mammal or a bird before reaching humans, he said.

Gibbs and two colleagues analyzed the publicly available sequences of hundreds of amino acids coded by each of the flu virus’s eight genes. He said he aims to submit his three-page paper today for publication in a medical journal.

“You really want a very sober assessment” of the science behind the claim, Fukuda said May 11 at the WHO’s Geneva headquarters.

The U.S. Centers for Disease Control and Prevention in Atlanta has received the report and has decided there is no evidence to support Gibbs’s conclusion, said Nancy Cox, director of the agency’s influenza division. She said since researchers don’t have samples of swine flu viruses from South America and Africa, where the new strain may have evolved, those regions can’t be ruled out as natural sources for the new flu.

No Evidence

“We are interested in the origins of this new influenza virus,” Cox said. “But contrary to what the author has found, when we do the comparisons that are most relevant, there is no evidence that this virus was derived by passage in eggs.”

The WHO’s collaborative influenza research centers, which includes the CDC, and sites in Memphis, Melbourne, London and Tokyo, were asked by the international health agency to review the study over the weekend, Fukuda said. The request was extended to scientists at the Food and Agriculture Organization in Rome, the World Organization for Animal Health in Paris, as well as the WHO’s influenza network, he said.

“My guess is that the picture should be a lot clearer over the next few days,” Fukuda said. “We have asked a lot of people to look at this.”

Lab Escape

Gibbs wrote or co-authored more than 250 scientific publications on viruses during his 39-year career at the Australian National University in Canberra, according to biographical information on the university’s Web site.

Swine flu has infected 5,251 people in 30 countries so far, killing 61, according to the WHO. Scientists are trying to determine whether the virus will mutate and become more deadly if it spreads to the Southern Hemisphere and back. Flu pandemics occur when a strain of the disease to which few people have immunity evolves and spreads.

Gibbs said his analysis supports research by scientists including Richard Webby, a virologist at St. Jude Children’s Research Hospital in Memphis, who found the new strain is the product of two distinct lineages of influenza that have circulated among swine in North America and Europe for more than a decade.

In addition, his research found the rate of genetic mutation in the new virus outpaced that of the most closely related viruses found in pigs, suggesting it evolved outside of swine, Gibbs said.

Some scientists have speculated that the 1977 Russian flu, the most recent global outbreak, began when a virus escaped from a laboratory.

Other Theories?

Identifying the source of new flu viruses is difficult without finding the exact strain in an animal or bird “reservoir,” said Jennifer McKimm-Breschkin, a virologist at the Commonwealth Science and Industrial Research Organization in Melbourne.

“If you can’t find an exact match, the best you can do is compare sequences,” she said. “Similarities may give an indication of a possible source, but this remains theoretical.”

The World Organization for Animal Health, which represents chief veterinary officers from 174 countries, received the Gibbs paper and is working with the WHO on an assessment, said Maria Zampaglione, a spokeswoman.

The WHO wants to know whether any evidence that the virus may have been developed in a laboratory can be corroborated and whether there are other explanations for its particular genetic patterns, according to Fukuda.

‘Wild Idea’

“These things have to be dealt with straight on,” he said. “If someone makes a hypothesis, then you test it and you let scientific process take its course.”

Gibbs said he has no evidence that the swine-derived virus was a deliberate, man-made product.

“I don’t think it could be a malignant thing,” he said. “It’s much more likely that some random thing has put these two viruses together.”

Gibbs, who spent most of his academic career studying plant viruses, said his major contribution to the study of influenza occurred in 1975, while collaborating with scientists Graeme Laver and Robert Webster in research that led to the development of the anti-flu medicines Tamiflu and Relenza, made by GlaxoSmithKline Plc.

“We were out on one of the Barrier Reef islands, off Australia, catching birds for the flu in them, and I happened to be the guy who caught the best,” Gibbs said. The bird he got “yielded the poo from which was isolated the influenza isolate strain from which all the work on Tamiflu and Relenza started.”

Gibbs, who says he studies the evolution of flu viruses as a “retirement hobby,” expects his research to be challenged by other scientists.

“This is how science progresses,” he said. “Somebody comes up with a wild idea, and then they all pounce on it and kick you to death, and then you start off on another silly idea.”

To contact the reporters on this story: Jason Gale in Geneva at [email protected]; Simeon Bennett in Singapore at [email protected].

Last Updated: May 12, 2009 21:16 EDT
Behold, happy is the man whom God correcteth: therefore despise not thou the chastening of the Almighty: For he maketh sore, and bindeth up: he woundeth, and his hands make whole ; He shall deliver thee in six troubles: yea, in seven there shall no evil touch thee. - Job 5

Offline TahoeBlue

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Interesting article....

Keywords: MITRE JASON

See below:
WMR has learned from a research scientist who has been working on the recreation of the 1918 flu that the genetic material has been re-engineered to synthetically create what is now known as the A/H1N1 virus, or as the Centers for Disease Control (CDC) calls it, the “novel flu.”

http://onlinejournal.com/artman/publish/article_4724.shtml

The history of the synthetic H1N1 flu virus and a not-so-rosy future
By Wayne Madsen
Online Journal Contributing Writer
May 21, 2009, 00:20
 
http://www.waynemadsenreport.com/
(WMR) -- The history of the extraction of the genetic material from the corpses of victims of the 1918 Spanish influenza virus who were buried in Arctic permafrost is part “X-Files” and part “Jurassic Park.”

After an unsuccessful 1951 mission, that involved U.S. biological warfare specialists, to extract 1918 Spanish flu genetic material in 1951 from a cemetery in the Inupiat Eskimo village of Brevig Mission, Alaska, scientists made another attempt, a successful one it turns out, in 1997.

Dr. Johan Hultin, from the State University of Iowa, successfully extracted genetic material from the corpse of an obese 30-something female who died from the Spanish flu in 1918, along with 85 percent of Brevig Mission’s (called Teller Mission in 1918) villagers in a single week. The pandemic killed at least 50 million people around the world.

Once the Spanish flu genetic material was obtained from the lungs, spleen, liver, and heart of the Eskimo woman’s corpse, scientists, in a scene reminiscent of the fictional movie “Jurassic Park,” in which genetic material from extinct dinosaurs is used to bring the creatures back to life, recreated the long-since dead 1918 Spanish flu in a U.S. government-funded laboratory. The woman’s organs were cut into one-inch cubes and shipped to the Armed Forces Institute of Pathology in Rockville, Maryland, where the virus’s genetic RNA material was identified and the 1918 Spanish flu was successfully brought back to life.

The search for the frozen bodies of 1918 flu victims was not limited to Alaska. Another team of scientists, acting like Dr. Frankenstein’s “Igor,” set out to dig up the graves of miners who died from the flu in the remote Norwegian mining village of Longyearbyen in Spitsbergen, which lies north of the Arctic Circle.

WMR has learned from a research scientist who has been working on the recreation of the 1918 flu that the genetic material has been re-engineered to synthetically create what is now known as the A/H1N1 virus, or as the Centers for Disease Control (CDC) calls it, the “novel flu.”

The A/H1N1 influenza, which contains genetic material from two strains of swine flu, two strains of human flu, and a single strain of avian flu, has, according to the World Health Organization (WHO), infected, as of May 13, a total of 4,880 people in North America: 2,059 in Mexico; 2,535 in the United States, and 286 in Canada. There have been 56 reported deaths from the flu in Mexico, three in the United States, and one in Canada.

WMR has learned from an A/H1N1 researcher that the current “novel” flu strain is mutating rapidly in humans but no animals have contracted the virus. The enzyme in A/H1N1, as with all influenza A viruses, is called a polymerase. Scientists have calculated the molecular clock of A/H1N1 form the virus’s polymerase rate. Because of the rapid mutation of the virus and the fact that, unlike 1918, rapid global transportation is now the norm, scientists are predicting that the molecular clock of the A/H1N1 virus, coupled with modern transportation, means that almost all the countries of the world will experience an A/H1N1 outbreak within the next few months.

What is different about A/H1N1 is that, unlike other new strains of viruses that rapidly mutate upon emerging and then slow down mutation and then stop entirely, the “novel” or incorrectly-named “swine flu” is showing no signs yet of slowing down its mutation rate and that, according to scientists who worry about A/H1N1 being synthetically-generated, does not happen in nature.

In 2006, at a summit meeting in Cancun, Mexico, President George W. Bush, Canadian Prime Minister Stephen Harper, and Mexican President Vicente Fox agreed for their nations to coordinate their response to avian flu, which was spreading in Asia. National Public Radio, on April 2, 2006, ran a segment on how bird flu wreaked havoc in 1918 in Brevig Mission. NPR’s Weekend Edition ran a report from Brevig Mission by Lori Townsend of Alaska Public Radio: “The grave has been opened twice by the same pathologist. In 1951, Johann Hultin convinced village elders to allow him to take tissue samples from bodies buried in permafrost. His lab attempts to map the virus were unsuccessful, but he returned in 1997, and when he did, he was once again given permission to re-open the grave.”

WMR has learned from a journalist from Anchorage who covered the 1997 grave exhumation that there was CIA personnel with the team of scientists. Inuit elders of Brevig Mission argued that digging up the graves of the flu victims would release evil spirits. However, money allegedly changed hands between the U.S. government research team and some of the elders, so permission to dig up the graves was granted.

NPR and Alaska Public Radio was reporting what was extracted from the 1918 flu victim’s corpse was the H5N1 avian flu virus, but that was erroneous. Or was it? If what was extracted from the dead woman’s body in Brevig Mission was used to synthetically create the current A/H1N1 virus, there is a strain of avian flu in the virus. But the current A/H1N1 virus also contains swine and human flu strains.

What has been relayed by the researcher is that the original 1918 virus was the H1N1 virus. In Bio-safety level 3 (BSL-s) laboratory work that was largely classified, the virus was artificially combined with common H3N2 and a minor gene splice from the H5N1 Eurasian avian flu strain.

The avian flu or H5N1 virus that struck Asia in 2006 contained some genetic mutations of the 1918 virus. And scientists researching pandemic flu strains have, since the recreation of the 1918 flu, been playing fast and loose with flu samples. On April 17, 2005, The Washington Post reported that Meridian Bioscience, which was under contract to the College of American Pathologists, accidentally distributed the pandemic H2N2/Japan flu strain, as part of a flu testing kit, to influenza laboratories around the world. WHO ordered the labs to immediately destroy the flu sample because it was worried about an accidental release of the pandemic virus, resulting in a global health crisis. In 1957, H2N2 killed a million people around the world.

The Post’s article, by Wendy Orent, states that scientists were working to create an artificial strain of the 1918 virus: “[Scientists] can combine some 1918 genes either with laboratory strains that have been adapted to grow in mice, which don’t normally catch human flu, or with ordinary human flu strains to yield new artificial strains. Then the researcher infects mice with his new strain. Strains using three of the 1918 genes are already known to kill mice.”

The same Post article quotes Peter B. Jahrling, the chief scientist at the National Institute of Allergy and Infectious Diseases, about the danger of the virus recreation research. Jahrling stated the research was like ”looking for a gas leak with a lighted match.” The article continues: “What concerns Jahrling and Brown, among others, is that experiments involving 1918 genes are not being carried out under the highest biosafety level, BSL-4. While most of the scientists use what is known as BSL-3 plus, or enhanced, conditions, they do not use space suits, chemical showers or gas-tight cabinets in their work.”

Lastly, the article has a stark warning regarding the 1918 flu reconstruction at the military laboratory in Rockville, research led by Dr. Jeffery Taubenberger. The article states: “Even more disturbing is what may happen when Taubenberger publishes the remaining three gene sequences. Then the entire 1918 flu could be built from scratch by anyone, anywhere, who has sufficient resources and skill. It is quite conceivable that resurrected 1918 flu could someday be used as a bioterrorist agent.”

In a January 29, 2006, New York Times article by Jamie Shreeve, titled “Why Revive a Deadly Flu Virus?,” it is reported that the 1918 flu had been successfully revived. The article states: “In October, a team of scientists, [CDC’s Terrence] Tumpey among them, announced that they had recreated the extinct organism from its genetic code -- essentially the scenario played out in the movie ‘‘Jurassic Park,’’ albeit on a microbial scale. In the movie, the scientists’ self-serving revivification of dinosaurs leads to mayhem and death . . . How dangerous is the 1918 virus to today’s population? Its genetic code is now in public databases, where other researchers can download it to conduct experiments. Scientists from the University of Wisconsin and the National Microbiology Laboratory in Canada have already collaborated to reconstruct the virus from the publicly available sequence. How easy would it be for a bioterrorist to exploit the same information for malevolent ends?”

The article details how the 1918 genetic material was extracted and who worked on the project: “The resurrection of the 1918 influenza virus was a team effort engaging the resources of the C.D.C. in Atlanta, an obscure military pathology lab outside Washington, D.C., an esteemed group of influenza experts at Mount Sinai School of Medicine in New York and one elderly Swede. Though the story has been told before, it is impossible not to begin with the Swede. In 1950, Johan Hultin, then a 25-year-old graduate student at the University of Iowa, was searching for a Ph.D. topic when he heard a visiting virologist say that the only way to solve the mystery of the 1918 pandemic would be to recover the virus from a victim who had been buried in permafrost.”

There has been yet another secretive U.S. government group involved in researching bio-warfare agents like influenza. Known simply as JASON, the group consists of civilian scientists, the top experts in their fields and a number of Nobel laureates, who meet periodically and issue reports, many of which are classified. JASON has been in existence for 40 years and is thought to be a follow-on to the Manhattan Project, the top secret scientific group that created the atomic bomb during World War II. In fact, some of JASON’s earliest members helped to design both the atomic and hydrogen bombs. Its first three members were scientists at Los Alamos National Laboratory, the home of the Manhattan Project.

Operating under the aegis of the MITRE Corporation, a federally-funded contracting entity, JASON scientists primarily met in the highly-secured Building 29 at 3550 General Atomics Court in San Diego. The location is the address of the Torrey Pines Institute. Funded by the Defense Advanced Research Projects Agency (DARPA), JASON also has links, according to distribution lists on JASON reports, to the CIA. The CIA maintains an element called the IC [Intelligence Community] JASON Program under the Chief Technical Officer. Traditionally, JASON self-selects its members from a number of academic disciplines. However, JASON almost lost its funding a few years ago, when, after issuing a report critical of the Bush administration’s ballistic missile defense program, DARPA attempted to force three new members, obviously political overseers, on to the JASON membership rolls. DARPA’s chief, Tony Tether, pulled funding for JASON, forcing the group for the first time since its inception in 1959 to look for another Pentagon sponsor. The ballistic missile defense program, also called Star Wars II, was a personal pet project of Secretary of Defense Donald Rumsfeld.

JASON survived when DARPA’s parent orgzniation, the Pentagon’s Directorate for Defense Research and Engineering (DDR&E), provided JASON with direct funding, an indication of the power enjoyed by the secretive JASON organization. JASON also has other federal government sponsors, including the Department of Energy.

JASON is also very much involved in issues of biological warfare. JASON produced a report on Civilian Biodefense in January 2000, which was highly redacted when released. Even the names of the report’s authors and the information on four bio-warfare scenarios is completely blacked out, except for a discussion of a 1947 smallpox incident in Scenario Two. The report also states that the CIA’s Clandestine Measurement and Signatures Intelligence (MASINT) Operations Center and Counter-Proliferation Center were interested in biological weapons intelligence collection and signatures. A section of the report on “Managing Civilian Response” to a bio-war attack is also completely redacted, as is a section on domestic intelligence. A page on the anthrax threat references “psychological BW [biological weapons] warfare.” The JASON report was completed almost two years before anthrax attacks all but suspended the work of Congress after 9/11 and saw the quick passage of the USAPATRIOT Act.

http://www.waynemadsenreport.com/downloads/20090513/download

The JASON report also discusses the mining of medical data, including patient billing records, to find out if a disease outbreak has occurred and how far and what direction it is spreading by examining “spatiotemporal patterns,” including “averaging statistics for humans traveling globally.”

In fact, the JASON Civilian Biodefense report mirrors, in many respects, the analysis being currently conducted by medical intelligence (MEDINT) agencies around the world on the outbreak and spread of A/H1N1. And that begs the question: is A/H1N1, artificially-developed by U.S. government scientists, the real thing or a test run for something much worse?

SIDEBAR:

The JASON report on bio-war discusses “managing civilian response.” That also appears be a major concern of the CDC on A/H1N1 at the present time judging from the following internal CDC memo obtained by WMR (note that “swine flu” is being referred to as the “novel H1N1 flu”):

From: CDC Announcements
Sent: Monday, May 11, 2009 10:31 AM
To: CDC All - [REDACTED]

Subject: Public Inquires Regarding Novel H1N1 Flu – CDC-INFO

Public Inquires Regarding Novel H1N1 Flu – CDC-INFO

The CDC National Contact Center, CDC-INFO, is available to assist CDC programs in responding to calls and emails related to the novel H1N1 flu. CDC-INFO maintains current content for phone and email responses; maintains records of calls/emails; collects and analyzes quality assurance and customer satisfaction data; and provides on-demand reports for program partners.

If the general public is contacting you with questions related to the novel H1N1 outbreak, we encourage you to direct those inquires you receive to CDC-INFO. CDC-INFO representatives are available to respond to inquiries 24 hours, 7 days a week via email and phone, in English and Spanish. Emails should be forwarded to [email protected]. Telephone inquiries may be routed to 1-800-CDC-INFO (1-800-232-4636).

If you have any questions regarding this email, or for assistance in routing public inquiries, please contact [email protected].

CDC-INFO’s Novel H1N1 Flu Response

Since April 22, 2009, CDC-INFO has answered more than 29,000 phone and email inquiries from the general public and health care professionals in support of CDC’s novel H1N1 flu response. As of Friday, May 8, 2009, the average hold time for phone calls related to novel H1N1 flu was less than 5 seconds. To date, the states with the highest number of phone inquiries are: California, Texas, New York, Florida, and Georgia.

On Thursday, April 30, 2009, CDC-INFO answered the highest number of inquiries on a single topic in its 4-year history, with 3,127 calls and emails answered related to the novel H1N1 outbreak.

As of May 5, 2009, 75 percent of survey respondents gave CDC-INFO their highest satisfaction rating for the novel H1N1 flu-related services they received.

Supporting CDC’s Mission

The CDC-INFO National Contact Center (1800-CDC-INFO or [email protected]) supports CDC’s mission by providing a single trusted source of accurate, timely, consistent, and science-based information for the general public, healthcare providers and public health partners. Information is available on more than 400 CDC health and safety topics, disease prevention, and health promotion information through phone, TTY, and email. CDC-INFO provides critical health information to vulnerable populations, including those without access to CDC’s internet resources or those with low health literacy.

Previously published in the Wayne Madsen Report.

Copyright © 2009 WayneMadenReport.com

Wayne Madsen is a Washington, DC-based investigative journalist and nationally-distributed columnist. He is the editor and publisher of the Wayne Madsen Report (subscription required).
Behold, happy is the man whom God correcteth: therefore despise not thou the chastening of the Almighty: For he maketh sore, and bindeth up: he woundeth, and his hands make whole ; He shall deliver thee in six troubles: yea, in seven there shall no evil touch thee. - Job 5

Offline TahoeBlue

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Quote
Just in Time for a North American - Global Pandemic?

So now we have S-P / Merck  major Animal Health vaccine manufacturer and sanofi pasteur  the number one human vaccine manufacturer and BIRMEX a "shadowy" Mexican govermental company.

Sanofi-aventis invests €100 million in new facility in Mexico

http://www.worldpharmanews.com/content/view/719/30/
Sanofi-aventis invests €100 million in new facility in Mexico
    
Thursday, 12 March 2009  
Sanofi-aventis (EURONEXT: SAN and NYSE: SNY), has announced the signing of an agreement with the Mexican authorities to build a € 100 million facility to manufacture influenza vaccine in Mexico. The announcement was made during a ceremony attended by Felipe Calderon, President of Mexico, and Nicolas Sarkozy, President of France, who was in Mexico City for a State visit.

Now on top of that Sanofi also has a brand new plant starting up THIS YEAR in the U.S. How could they have known?:

http://whyy.org/cms/news/health-science/2009/06/18/sanofi-will-donate-h1n1-vaccine/10620
Sanofi will donate H1N1 vaccine
Thursday, June 18th, 2009 By: Kerry Grens [email protected]

Sanofi Aventis, which has its North American vaccine plant in Swiftwater, PA, says it will donate 100 million doses of H1N1 influenza vaccine to the World Health Organization, once the shot is developed. The company can accommodate additional vaccine production for this new strain of the virus, while continuing to make seasonal flu shots, because of its new plant that went online this year. (Photo: CDC)

Baxter, GlaxoSmithKline, and MedImmune are among the handful of other companies developing a vaccine against the H1N1 pandemic flu. Novartis announced last week that it successfully produced the first batch of vaccine. The shot still needs to go through testing, approval, and mass production before it will be available. Companies expect vaccines to be ready by the fall.

http://whyy.org/cms/news/health-science/2009/05/06/sanofi-to-ramp-up-flu-shot-production/8175
Sanofi to ramp up flu shot production
Wednesday, May 6th, 2009  By: Kerry Grens [email protected]

Sanofi Pasteur’s new facility could help combat swine flu next fall, as well as significantly increase the number of regular flu shots made in the US. The Food and Drug Administration Wednesday gave Sanofi Pasteur the okay to launch its newest facility to make vaccines in time for next year’s flu season. The Swiftwater-based company already provides 50 million flu shots annually in the US. Sanofi spokeswoman Donna Cary says the new facility could add another 100 million doses.

Now we have companies with no customers/contracts making vaccine:

http://www.chicagotribune.com/news/wtic-swine-flu-vaccine-0616,0,6506487.story

Meriden Company Producing Swine Flu Vaccine
The Associated Press  
June 24, 2009

MERIDEN, Conn. (AP) - A Connecticut company says it is producing tens of thousands of doses of a swine flu vaccine.

Protein Sciences Corp. of Meriden says it has been producing a vaccine aimed at the H1NI virus and expects to have 100,000 doses done this week.

The company says it doesn't yet have a customer for the vaccine, PanBlok, but says the vaccine should be available for human clinical trials in July. Company officials are in talks with the World Health Organization about human testing in Mexico, the U.S. and Australia.
-----
Now this company seems to be a Industrial Complex player.... private company....

http://investing.businessweek.com/businessweek/research/stocks/private/snapshot.asp?privcapId=159397

Company Overview
Protein Sciences Corporation, a biotechnology company, engages in developing and manufacturing recombinant human and veterinary vaccines, therapeutics, and diagnostics utilizing its baculovirus expression vector system technology. Its products include influenza vaccines, recombinant neuraminidase, SARS vaccines, and novel adjuvants. The company also offers protein production services; cGMP manufacture of commercial material; complex proteins for research and diagnostic applications; baculovirus protein expression kits; insect cell produced recombinant proteins for use in laboratory animals or for in vitro testing; and SARS research antigens; and influenza research antigens...

Key developments for Protein Sciences Corporation
Emergent BioSolutions Inc.'s Subsidiary Files Lawsuit Against Protein Sciences Corporation
06/9/2009
On June 8, 2009, a subsidiary of Emergent BioSolutions Inc. filed a lawsuit against Protein Sciences Corporation for possession of substantially all of PSC's assets, which serve as the collateral securing a $10 million loan that Emergent made to PSC in connection with a planned purchase of PSC's assets in 2008. Emergent also intends to proceed with its pending lawsuits against PSC and its management team, which include claims for breach of contract, fraud, and unfair business practices. In 2008, Emergent entered into a loan and security agreement and a related promissory note with PSC, pursuant to which Emergent provided PSC with $10 million in funding intended to keep PSC operating through the closing of an asset purchase planned for June 2008. The loan is secured by substantially all of PSC's assets, including its intellectual property. At this time, the company believes that the current value of the collateral is sufficient to cover the amount of the debt.

Protein Sciences Inks Deal to Run A Manufacturing Facility in the Country [Mexico]
05/7/2009
Protein Sciences Corporation announced that it has signed a deal with the Mexican regulator to run a manufacturing facility in the country. The company did not disclose the terms and conditions of the deal. The company has not committed to making Influenza A H1N1 (swine 'flu) vaccine, however the factory may be used to make a seasonal 'flu vaccine that the firm hopes to launch in the country this year.
Behold, happy is the man whom God correcteth: therefore despise not thou the chastening of the Almighty: For he maketh sore, and bindeth up: he woundeth, and his hands make whole ; He shall deliver thee in six troubles: yea, in seven there shall no evil touch thee. - Job 5

Offline TahoeBlue

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This article addresses multiple facets of the vaccine scam....http://www.newsmax.com/health/vaccine_swine_flu/2009/07/07/232717.html
Vaccine May Be More Dangerous Than Swine Flu

Tuesday, July 7, 2009 9:54 AM
By: Dr. Russell Blaylock

An outbreak of swine flu occurred in Mexico this spring that eventually affected 4,910 Mexican citizens and resulted in 85 deaths. By the time it spread to the United States, the virus caused only mild cases of flu-like illness.

Thanks to air travel and the failure of public health officials to control travel from Mexico, the virus spread worldwide. Despite predictions of massive numbers of deaths and the arrival of doomsday, the virus has remained a relatively mild disease, something we know happens each year with flu epidemics.

Worldwide, there have only been 311 deaths out of 70,893 cases of swine flu. In the United States, 27,717 cases have resulted in 127 deaths. Every death is a tragedy, but such a low death rate should not be the basis of a draconian government policy.

It is helpful to recall that the Centers for Disease Control with the collusion of the media, constantly tell us that 36,000 people die from the flu each year, a figure that has been shown to be a lie. In this case, we are talking about 300 plus deaths for the entire world.

This virus continues to be an enigma for virologists. In the April 30, 2009 issue of Nature, a virologist was quoted as saying,“Where the hell it got all these genes from we don’t know.” Extensive analysis of the virus found that it contained the original 1918 H1N1 flu virus, the avian flu virus (bird flu), and two new H3N2 virus genes from Eurasia. Debate continues over the possibility that swine flu is a genetically engineered virus.

Naturally, vaccine manufacturers have been in a competitive battle to produce the first vaccine. The main contenders have been Baxter Pharmaceuticals and Novartis Pharmaceuticals, the latter of which recently acquired the scandal-ridden Chiron vaccine company (merged with Novartis). Both of these companies have had agreements with the World Health Organization to produce a pandemic vaccine.

The Baxter vaccine, called Celvapan, has had fast track approval. It uses a new vero cell technology, which utilizes cultured cells from the African green monkey. This same animal tissue transmits a number of vaccine-contaminating viruses, including the HIV virus.

The Baxter company has been associated with two deadly scandals. The first event occurred in 2006 when hemophiliac components were contaminated with HIV virus and injected in tens of thousands of people, including thousands of children. Baxter continued to release the HIV contaminated vaccine even after the contamination was known.

The second event occurred recently when it was discovered that Baxter had released a seasonal flu vaccine containing the bird flu virus, which would have produced a real world pandemic, to 18 countries. Fortunately, astute lab workers in the Czech Republic discovered the deadly combination and blew the whistle before a worldwide disaster was unleashed.

Despite these two deadly events, WHO maintains an agreement with Baxter Pharmaceuticals to produce the world’s pandemic vaccine.

Novartis, the second contender, also has an agreement with WHO for a pandemic vaccine. Novartis appears to have won the contract, since their vaccine is near completion. What is terrifying is that these pandemic vaccines contain ingredients, called immune adjuvants that a number of studies have shown cause devastating autoimmune disorders, including rheumatoid arthritis, multiple sclerosis and lupus.

Animal studies using this adjuvant have found them to be deadly. A study using 14 guinea pigs found that when they were injected with the special adjuvant, only one animal survived. A repeat of the study found the same deadly outcome.

So, what is this deadly ingredient? It is called squalene, a type of oil. The Chiron company, maker of the deadly anthrax vaccine, makes an adjuvant called MF-59 which contains two main ingredients of concern—squalene and gp120. A number of studies have shown that squalene can trigger all of the above-mentioned autoimmune diseases when injected.

The MF-59 adjuvant has been used in several vaccines. These vaccines, including tetanus and diphtheria, are the same vaccines frequently associated with adverse reactions.

I reviewed a number of studies on this adjuvant and found something quite interesting. Several studies done on human test subjects found MF-59 to be a very safe immune adjuvant. But when I checked to see who did these studies, I found—to no surprise—that they were done by the Novartis Pharmaceutical Company and Chiron Pharmaceutical Company, which have merged. They were all published in “prestigious” medical journals. Also, to no surprise, a great number of studies done by independent laboratories and research institutions all found a strong link between MF-59 and autoimmune diseases.

Squalene in vaccines has been strongly linked to the Gulf War Syndrome. On August 1991, Anthony Principi, Secretary of Veterans Affairs admitted that soldiers vaccinated with the anthrax vaccine from 1990 to 1991 had an increased risk of 200 percent in developing the deadly disease amyotrophic lateral sclerosis (ALS), also called Lou Gehrig’s disease. The soldiers also suffered from a number of debilitating and life-shortening diseases, such as polyarteritis nodosa, multiple sclerosis (MS), lupus, transverse myelitis (a neurological disorder caused by inflammation of the spinal cord), endocarditis (inflammation of the heart’s inner lining), optic neuritis with blindness and glomerulonephritis (a type of kidney disease).

The second ingredient, and one that greatly concerns me, is called gp120, a glycoprotein. Researchers found when it was mixed with squalene, the glycoprotein became strongly antigenic—that is, it produced a powerful and prolonged immune response to the vaccination. In fact, their studies show that with each dose, the intense immune reaction lasts over a year.

Now for the shocker—the glycoprotein-gp120, a major component of MF-59 vaccine adjuvant, is the same protein fragment isolated from the HIV virus that is responsible for the rapid dementia seen in AIDS patients.

Studies have shown that when gp120 is taken up by the microglia cells in the brain, it causes intense inflammation and makes the brain subject to excitotoxic damage—a process called immunoexcitotoxicity. This is also the cause of the MS and optic neuritis associated with vaccines that contain MF-59.

So, how would the gp120 get into the brain? Studies of other immune adjuvants using careful tracer techniques have shown that they routinely enter the brain following vaccination. What most people do not know, even the doctors who recommend the vaccines, is that most such studies by pharmaceutical companies observe the patients for only one to two weeks following vaccination—these types of reactions may take months or even years to manifest.

It is obvious that the vaccine manufacturers stand to make billions of dollars in profits from this WHO/government-promoted pandemic. Novartis, the maker of the new pandemic vaccine, recently announced that they would not give free vaccines to impoverished nations—everybody pays.

One must keep in mind that once the vaccine is injected, there is little you can do to protect yourself—at least by conventional medicine. It will mean a lifetime of crippling illness and early death.

There are much safer ways to protect oneself from this flu virus, such as higher doses of vitamin D3, selective immune enhancement using supplements, and a good diet.

© 2009 Newsmax. All rights reserved.
Behold, happy is the man whom God correcteth: therefore despise not thou the chastening of the Almighty: For he maketh sore, and bindeth up: he woundeth, and his hands make whole ; He shall deliver thee in six troubles: yea, in seven there shall no evil touch thee. - Job 5

Mike Philbin

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if noone's gonna say it, I'll say it

DEATH FACTORIES